IRF7 can be activated by weakly virulent Mycobacterium tuberculosis, acting synergistically with IRF3 to increase IFN-I production and thus control infection.IRF7 can be inhibited by OASL, a negative regulator of IFN-I activated by strongly virulent Mycobacterium tuberculosis, to suppress inhibition and produce a cytokine storm that ultimately leads to macrophage death. The gene discussed is OASL; the disease is infection.