These findings suggest that the affected MAP9, together with mutant RPGRIP1, is deprived of critical roles in cilia organization and maintenance resulting in altered cilia structure and function giving rise to early onset and accelerated disease progression in the RPGRIP1ins44/ins44MAP9aff/aff double homozygote cone-rod dystrophy canine model. This evidence concerns the gene MAP9 and Cone rod dystrophy.