In fact, overexpression of deacetylase-active HDAC6 inhibited the α-tubulin acetylation of MTs by HIV-1, preventing HIV-1 Env-mediated membrane fusion and infection without affecting the expression and distribution of HIV-1 receptors (i.e., CD4, CCR5, and CXCR4), while the knockdown of HDAC6 expression or inhibition of its tubulin-deacetylase activity strongly enhanced HIV-1 Env-mediated cell-to-cell fusion (syncytia formation (virus-mediated fused giant multinucleated cells)) and HIV-1 infection of primary CD4+ T cells [164] (Figure 3). The gene discussed is CXCR4; the disease is infection.