GJD2 and retinitis pigmentosa 1: In summary, our study provides the first conclusive evidence that a Cx36-dependent gap junction-mediated bystander effect, postulated by Ripps [8], is not involved in secondary cone degeneration in mouse models for RP as the deletion of Cx36 on the cone side of the rod-cone gap junction had no effect on the secondary death of genetically healthy cones.