Alternatively, taking into account that the sole activation of VPAC1 facilitates HIV-1 infection in CD4+ T cell lines (27), one could explain the HIV-1 promoting effect by VIP at 100 nM due to a possible preferential engagement of VPAC1 at high VIP concentrations, although it has been described that the affinity of VIP for its receptors VPAC1 and VPAC2 is similar [4]–[7]. The gene discussed is CD4; the disease is HIV-1 infection.