TB-LM induces higher miR-125b expression that targets the TNF mRNA and inhibits TNF biosynthesis through inhibition of TLR-2–mediated miR-155 expression, whereas M. smeg LM induces miR-155 expression and downregulates miR-125b and SHIP1, thereby increasing-PI3K/Akt signaling and TNF production followed by an enhanced proinflammatory response (50). The gene discussed is TNF; the disease is tuberculosis.