Considering that (i) HIV-1 stabilizes acetylated microtubules during the initial HIV-1 Env/CD4 contacts to favour pore fusion formation and infection [44, 46, 90], and (ii) HDAC6 plays an anti-HIV-1 replicative activity regulating this process [44–46], in conjunction with the impairment of both Tat proviral function (by HDAC6-mediated Tat deacetylation) [91] and the proposed HDAC6/A3G restriction complex, the regulation of HDAC6 in immune cells could represent a new way to overcome HIV-1 Vif proviral functions and control HIV-1 infectiveness. This evidence concerns the gene HDAC6 and infection.