Regulation of chemotaxis by mitochondria, mTOR, and purinergic signaling. Phase 1, trigger: FPR stimulation induces mTORC1 signaling and mitochondrial activation and ATP formation. Phase 2, warm up: ATP release through panx1 triggers P2Y2 receptors that stimulate mTORC2 and enhance mitochondrial activity and ATP production. This promotes actin polymerization and pseudopod protrusion at the front of cells. Phase 3, shut-down: ATP is hydrolyzed to adenosine by ectonucleotidases (ENTPD) on the cell surface, resulting in the stimulation of A2a adenosine receptors at the back of cells. This results in cAMP accumulation and the inhibition of FPR/P2Y2-mediated mTORC signaling and mitochondrial activation, leading to uropod retraction at the back. We propose a purinergic LEGI model, with phases 1 and 2 representing local excitation and phase 3 representing global inhibition.