FcγRIIa may be particularly effective in phagocytosis-induced activation of myeloid cells by immune complexes in HIV-1 infection, because, unlike other activatory FcγRs (FcγRI and FcγRIIIa), signal transduction via the immunoreceptor tyrosine-based activation motif (ITAM) of FcγRIIa does not require the FcR common γ-chain adaptor molecule, which is depleted by HIV-1 infection [60]. Here, FCGR3A is linked to HIV-1 infection.