Increased levels of pro-inflammatory cytokines, such as Interleukin (IL)-6, IL-7, IFN-α, and TNF-α; increased chemokines, such as IP-10 (CXCL10); and the expression of the activation markers CD69 and CD38/HLA-DR on T cells during HIV-1 infection are characteristic signs of continuing immune activation and may contribute to mechanisms hindering T cell reconstitution [4,6,7]. The gene discussed is IFNA1; the disease is HIV-1 infection.