The N-terminal calponin homology domain of IFT81 interacts with the N-terminal domain of IFT72 to form a tubulin binding module required for transportation of tubulin during ciliogenesis.8,19,20 Like other IFT-B core members, mutations in IFT81 have been observed to cause syndromic ciliopathies featuring renal medullary cysts, paraxial polydactyly, early onset rod-cone dystrophy, cerebellar atrophy, and intellectual disability.21 However, thus far, the association between mutations in IFT81 and nonsyndromic human disease has not been reported. The gene discussed is IFT81; the disease is Rod-cone dystrophy.