The homologous REP-2, encoded by CHML, shares redundant function with REP-1, and hypotheses to explain the eye-exclusive phenotype in choroideremia have included the possibility of specific Rabs with particular importance in the eye that have less efficient prenylation with REP-2, or higher REP-2 expression compensating in non-ocular tissues [17]. Here, CHML is linked to choroideremia.