Vga9 mice are a strain with blind, deaf, and albino phenotypes. This poor little animal is indeed legendary in the history of pigment cell and melanoma research and changed many researchers' careers.  However, its generation was purely accidental. 

In the late 1980s, Harold Gainer and James Battey, both at National Institue of Neurological Disorders and Stroke (NINDS) at that time, were interested in the question of promoter regulation of the arginine vasopressin (Avp) and oxytocin (Oxt) genes. Yoshinobu Hara (visiting fellow in Gainer’s laboratory) and Battey constructed two targeting vectors for making transgenic (Tg) mice: putative promoter regions of Avp or Oxt connected with bacterial β-galactosidase and the human AVP 3′ end. The purpose was to find the tissues exhibiting β-galactosidase activity (by Xgal labeling) that suggested activation of either genes. In 1988, by pronuclear injection into mice with dark coat color, Dr. Heinz Arnheiter generated ten Oxt and eight Avp transgenic founders. Unfortunately, none of the transgenic offspring showed Xgal labeling because the β-galactosidase gene contained a frameshift mutation that was not recognized before the mice were made. Therefore, Heinz and Yoshinobu turned to in situ hybridization. However, none of the offspring expressed transgenic β-galactosidase RNA in brain nuclei where Avp and Oxt were known to be expressed.

Considering dose effect of a transgene, Yoshinobu tried to get homozygous Tg mice by  intercrossing the offspring of each line, but still none of results showed Xgal labeling.  To his surprise,  Yoshinobu found white mice with small red eyes among the offspring of the Avp line from founder #1034, which he called vga-9 (#1034 was the ninth mouse inspected from the first injection of the vasopressin/β-galactosidase/human AVP transgene). He soon realized that these mice looked like mi mice, a trait similar to microphthalmia, a rare developmental disorder of the eye in which one or both eyes are abnormally small, in human. The patients usually also have problems in pigmentation and hearing. By crossing with mi heterozygotes, vga-9/mi mice all looked like mi/mi homozygous mice. These mice attracted attentions from experts in different fields. Heniz and his collaborators found that Vga-9 mice had defect mast cells and no melanocytes.  All these results  confirmed that vga-9 was indeed a mutation at the microphthalmia locus.

When Heinz told Nancy Jenkins from the Mammalian Genetics Laboratory, the ABL-Basic Research Program, NCI-Frederick, about these mice, she immediately expressed the interest to collaborate and clone the gene that caused these phenotypes. With persistence, skill, and a blessing of luck, Colin Hodgkinson, the visiting fellow in Heinz's lab, cloned the flanking regions of the transgene. In these clones, Nancy Jenkins and Neal Copland's group identified the entire open reading frame of a novel member of the E-box binding basic-helix-loop-helix-leucine zipper family of transcription factors. Hienz and Nancy's groups published it in Cell 1993, termed this factor Microphthalamia-associated Transcription Factor, MITF. 

This gene changed the research career of Heinz, turning him from a virologist to a pigment cell researcher, as he stated: 

"Little did I know at the moment that this observation was the beginning of a new field of research and a switch of my career from 20 yr of virology to now nearly 20 yr of developmental biology."

For the following two decades since the discovery, Heinz identified functions of MITF and proved that MITF is the master regulator and melanocyte development. These studies also dramatically impacted melanoma research. It would not be overstated that MITF is the most important gene in pigment cell research, and all of these were originated from a failed time-consuming experiment. Heinz recalled:

"Had the experiment not been such a failure, the idea of systematically generating transgene-homozygotes might never have come up, and given the high costs of keeping laboratory mice, the vga-9 line might have been terminated long before the appearance of any white and small-eyed mouse."

Years later, MITF was renamed as "melanocyte inducing transcription factor". Heinz was not happy about it. He told me that the function of MITF is not limited to melanocytes but also many other cell types (such as mast cells as mentioned above). Moreover, traditionally, gene was named after the associated phenotypes or diseases. In that case, "microphthalamia associated" is more appropriate than "melanocyte inducing", as microphthalamia-associated phenotypes include much more than the shape of eyes, but also pigment cell change, neural symptoms, etc. The change of the name symbolized the current trend of disconnection between genetics and physiology.

Reference:

The discovery of the microphthalmia locus and its gene, Mitf. Pigment Cell & Melanoma Research (2010). https://onlinelibrary.wiley.com/doi/full/10.1111/j.1755-148X.2010.00759.x