Thus, expression of these cytotoxic molecules by M. tb-specific TSCM, TCM, and TEFF, in absence of granzyme B and perforin, may induce pro-inflammatory responses in macrophages at the site of infection, rather than mediate direct killing of M. tb-infected macrophages, which would require perforin to mediate entry of granzymes into infected cells. The gene discussed is PRF1; the disease is infection.