In the setting of HIV-1/Mtb co-infection, Mtb infection-mediated up-regulation of PPM1A followed by increased HIV-1 susceptibility results in a scenario that could provide the underlying molecular mechanism to explain previous reports that have shown increased HIV-1 replication at sites of Mtb infection in the lung [16], and in acutely Mtb-infected macrophages [17, 18]. The gene discussed is PPM1A; the disease is coinfection.