Therefore it seems likely that these two chemokine signalling pathways and maybe the innate immune status of myeloid cells might act as a modifier for CRB1 mutations in humans and thus contribute to the high phenotypic variability observed in patients with different CRB1 mutations that either lead to Lebers congenital amaurosis (LCA), early onset childhood retinal dystrophy or juvenile onset retinitis pigmentosa [54]. This evidence concerns the gene CRB1 and Leber congenital amaurosis.