Autophagy and endocytosis are two evolutionarily conserved catabolic processes that comprise vesicle trafficking events for the clearance of the sequestered intracellular and extracellular cargo. Both start differently but end in the same compartment, the lysosome. Mounting evidences from the last years have established the involvement of proteins sensitive to intracellular Ca(2+) in the control of the early autophagic steps and in the traffic of autophagic, endocytic and lysosomal vesicles. However, this knowledge is based on dispersed outcomes that do not set up a consensus model of the Ca(2+)-dependent control of autophagy and endocytosis. Here, we will provide a critical synopsis of insights from the last decade on the involvement of Ca(2+)-sensor proteins in the activation of autophagy and in fusion events of endocytic vesicles, autophagosomes and lysosomes.