To demonstrate that the impact of NFAT5 silencing on MTb-induced viral replication was a direct effect due to modulation of recruitment of NFAT5 to the HIV-1 LTR and not due to secondary, NFAT5-regulated effects, we set out to disrupt NFAT5 binding to the viral LTR in the context of HIV-1/MTb co-infection. The gene discussed is NFAT5; the disease is coinfection.