The hypothesis presented by Di Giosaffatte et al. depends on the presence of four conditions: (1) that REP1 predominantly binds RGGT prior to Rab proteins according to the ‘alternative model’, (2) that the truncated protein sequesters RGGT and impairs Rab prenylation in vivo as predicted by in silico domain analysis in order to cause a dominant negative effect, (3) that escape expression of CHM occurs at sufficient levels for this to be pathogenic to cause a carrier phenotype and (4) that this mechanism is concordantly pathogenic in males to cause choroideremia. The gene discussed is CHM; the disease is choroideremia.