Finally, CRISPR-targeting to disrupt Tyro3 in Mertk−/−V2 B6 ES cells and the generation of fully B6 Mertk−/−V2; Tyro3−/−V2 mice (Figure 2) unequivocally supported the notion that the retinal degeneration observed in 129 ES cell-derived Mertktm1Gkm/tm1Gkm mice required the simultaneous loss of function of MERTK and diminished expression of TYRO3 [46]. The gene discussed is TYRO3; the disease is retinal degeneration.