By utilizing simvastatin at drug concentrations compatible with clinical dosing (Cmax 1 μM) (26) to treat M. tuberculosis-infected human monocytic cells, we now show that the anti-tubercular activity of statins results from their cholesterol-lowering effects and the consequent regulation of the nutrient- and energy-sensing pathways regulated by the AMP-activated protein kinase (AMPK), the mechanistic target of rapamycin complex 1 (mTORC1), and the transcription factor EB (the AMPK-mTORC1-TFEB axis) in ways that promote autophagy and control of infection with intracellular pathogens. This evidence concerns the gene TFEB and infection.