My most important scientific contributions are framed in two areas of research: immunology and cancer. Among my various contributions in immunology, perhaps the most outstanding from an intellectual and subsequently translational point of view, has been the demonstration that the receptor for the antigen of T lymphocytes (TCR) undergoes conformational changes after the binding of antigens and agonistic antibodies (Cell, 2002). This discovery broke the existing dogma that the TCR did not undergo conformational changes, but rather signal transmission occurred through mere mechanisms of aggregation and/or molecular exclusion. This discovery has revolutionized the view of the TCR, perhaps the most important molecule in the functioning of the adaptive immune response. In fact, and just as an example, the TCR enables vaccines to work or for so-called "checkpoint inhibitors" to have anticancer activity. It is also part of the development of cancer therapy known as "CAR-T". We based the demonstration of the existence of conformational changes in the TCR on the observation that, as a consequence of antigen stimulation, the TCR exposes a sequence that recruits the adaptor protein Nck. This occurs through an SH3 domain of Nck that has a unique "pocket". This offered the opportunity to design molecules that interfere with the TCR-Nck binding. Following this idea, we designed, through an "in silico" procedure, a low molecular weight inhibitor to fit into that pocket and prevent the recruitment of Nck to the TCR, and therefore signal transmission. Such inhibitor, which we named AX024, proved to be effective through oral administration in various models of autoimmune diseases: psoriasis, Crohn's disease/ulcerative colitis, asthma, and multiple sclerosis (Sci. Transl. Med, 2016), all caused to a large extent by uncontrolled activation of T lymphocytes. This inhibitor and its entire family of derivatives were patented and led to the creation of the company Artax Biopharma Inc based in Boston MA. I am a founding member of Artax, I was its CSO and now I am a member of its Scientific Advisory Board. Artax has improved the initial compound with the lead AX158. This latter compound has completed all regulatory preclinical phases and Phase I. It is currently in Phase II for psoriasis treatment. If the drug meets expectations, it will be the first immunomodulatory drug, not immunosuppressive, acting on the TCR and with a possibility of use in practically all autoimmune diseases. The drug is administered orally, with only a daily dose and unaffected by food intake or not. In conclusion, it is a "First-in-class" drug for many reasons: it modulates TCR signaling and acts by inhibiting a protein-protein interaction, not an enzymatic activity, which distinguishes it from most pharmacological compounds currently in use. Our interest in characterizing TCR signaling molecules led us to identify not only Nck but also R-RAS2; obtaining novel and impactful results in cancer. R-RAS2 is a GTPase similar to the oncogene K-RAS, which, however, does not undergo activating mutations in practically any type of cancer. Perhaps for this reason, interest in R-RAS2 declined despite being discovered in 1990. Contrary to K-RAS and other similar GTPases, R-RAS2 has a high intrinsic activity of guanosine nucleotide exchange. This peculiarity led us to think that elevated levels of R-RAS2 expression, even in the absence of activating mutations, could cause cancer. Our work, based on the generation of a transgenic mouse that overexpresses the wild-type form of R-RAS2, demonstrated that this hypothesis is correct. In fact, we found that all mice develop chronic lymphocytic leukemia (CLL), a B-cell leukemia that is the most common in the West (Mol Cancer, 2022). This allowed us to translate these observations to humans, analyzing a cohort of patients with CLL. This study showed that more than 80% of patients overexpress non-mutated R-RAS2. Additionally, we found genetic markers in non-coding regions of the RRAS2 gene that are linked to this overexpression. Such markers can be used as a prognostic method as they are linked to worse survival. Currently, we are characterizing RRAS2 as the most frequently implicated gene (68%) in the development of breast cancer, especially in forms known as "triple-negative" and those linked to pregnancy. In addition to these two lines of research representing the pillars of my research career, we have been involved in the creation of a diagnostic test for immunity to SARS-CoV-2 that was patented and commercialized by a Spanish company during the recent pandemic (EMBO Mol Med, 2021). The method on which this test is based can be used for the evaluation of humoral response to any pathogen. In summary, I believe that my trajectory shows how research aimed at understanding basic mechanisms can be translated into clinical use. One of the products of this translation, AX158, has reached the Clinic, and another product, genetic markers of RRAS2, is in the process of materializing as a prognostic marker, in addition to pointing to R-RAS2 as a target for future therapies.