In particular, we discuss the mechanisms and signaling pathways (adenosine 5′-monophosphate [AMP]-activated protein kinase [AMPK], mammalian target of rapamycin [mTOR] kinase, Wnt, transcription factor EB [TFEB], cathelicidins, inflammation, endoplasmic reticulum [ER] stress, and autophagy-related genes [ATGs]) that would make autophagy-activating agents a potential host-directed therapeutic (HDT) or alternative to current tuberculosis (TB) chemotherapeutics. Here, MTOR is linked to tuberculosis.