This in turn may have important implications for future therapy development because (i) it expands the perimeter from apoptotic to other, alternative mechanisms which in turn may yield a number of novel targets for neuroprotective treatments (ii) the same non-apoptotic processes were observed in the two rhodopsin mutants as well as in the PDE6 mutant rd1 mouse and hence strongly improve the perspectives for a mutation-independent neuroprotective treatment of RP. The gene discussed is PDE6B; the disease is retinitis pigmentosa 1.