Functional intracellular Ca(2+) signaling is essential for the upregulation of 
the canonical mTOR-controlled autophagy pathway triggered by rapamycin or by 
nutrient deprivation. Moreover, modifications in the Ca(2+)-signaling machinery 
coincide with autophagy stimulation. This results in enhanced intracellular 
Ca(2+) signaling essential for driving the autophagy process. Yet, the 
mechanisms upstream (the players causing the changes in Ca(2+) signaling) and 
downstream (the targets of the altered Ca(2+) signals) of this Ca(2+)-dependent 
autophagy pathway remain elusive. Here, we speculate about these mechanisms 
based on our current knowledge.