CNGB3 and achromatopsia: As mutations in CNG channels are the most common cause of human achromatopsia (CNGB3 ≥ 50%, CNGA3 ≥ 25%), the demonstration of successful gene therapies by AAV vectors to rescue cone function in this model [18], [41], in CNGB3-mutant dogs [42] and in Cnga3-/- mice [19] provides key proof-of-principle for future achromatopsia clinical trials in humans.