Along the same line, epidemiological results associated the Δ32 CCR5 homozygous genotype with protection against the acquisition of HIV-1 [54-57], indicating that modulating CCR5 expression or function in HIV-infected individuals could help control progression of HIV infection, as occurs with maraviroc treatment; in despite of this, some Δ32 CCR5 homozygous individuals have become infected with HIV-1, indicating that this genotype may not be fully protective [58,59]. This evidence concerns the gene CCR5 and HIV infectious disease.