SAG and retinitis pigmentosa: However, a previously identified loss-of-function mutation in arrestin-113 is recessive, as the other perfectly normal allele is sufficient for function, in line with our earlier finding that as little as 4% of wild-type (WT) arrestin expression level is sufficient for maintaining rod health in mice.14 It is interesting that recently identified C147F mutation in the human arrestin-1 is dominant and causes retinitis pigmentosa.15 Thus, loss of function cannot explain the mechanism of action of this mutant arrestin-1.