HIV-1 variants with higher CCR5 affinities and lower sensitivities to CCR5 ligands can arise naturally during HIV-1 infection, because of the drop in the average levels of CCR5 available on target cells [40–44]; CCR5 inhibitor-resistant variants might, in principle, have a similar advantage over wild-type viruses under certain conditions. The gene discussed is CCR5; the disease is HIV-1 infection.