HIV-1 Tat protein induces transcriptional dysregulation with particular activation of IL-17 signalling pathways.24 Profound depletion of IL-17-producing T-helper (Th)17 cells is observed at mucosal barriers early after HIV-1 infection, leading to chronic immune activation.25 The combination of ongoing mucosal inflammation, HIV-1 replication, and M tuberculosis co-infection could result in heightened immune activation leading to constant triggering of the remaining IL-17A-producing cell populations during HIV–tuberculosis co-infection. The gene discussed is IL17A; the disease is HIV-1 infection.