Mycobacterium tuberculosis remains a global threat to human health yet the molecular mechanisms reg ulating immunity remain poorly understood. Cytokines can promote or inhibit mycobacteria l survival inside macrophages , and the underlying mechanisms represent potential targets for host - directed therapies . Here w e show t hat cytokine - STAT signaling promote s mycobacterial survival within macrophages by deregulatin g lipid droplets via ATG2 repression . I n Drosophila infected with Mycobacterium marinum , mycobacterium - induced STAT activity triggered by unpaired - family cytokines reduces Atg2 expression , permitting deregulation of lipid droplets. Increased Atg2 expression , or reduced macrophage triglyceride biosynthesis, normalize s lipid deposition in infected phagocytes and reduces numbers of viable intracellular mycobacteria. I n human macrophages, addition of IL - 6 promotes mycobacterial survival and BCG - induced lipid accumulation by a similar, but probably not identical, mechanism . Our results reveal Atg2 regulation as a mechanism by which cytokines can control lipid droplet homeostasis and consequently resistance to mycobacterial infection in Drosophila .