Functional intracellular Ca2+ signaling is essential for the upregulation of the canonical mTOR-controlled autophagy
pathway triggered by rapamycin or by nutrient deprivation. Moreover, modifications in the Ca2+-signaling machinery
coincide with autophagy stimulation. This results in enhanced intracellular Ca2+ signaling essential for driving the autophagy process. Yet, the mechanisms upstream (the players causing the changes in Ca2+ signaling) and downstream (the targets of the altered Ca2+ signals) of this Ca2+-dependent autophagy pathway remain elusive. Here, we speculate about these mechanisms based on our current knowledge.