Toxoplasma gondii, like all apicomplexan parasites, uses Ca2+signalling pathways to activate gliding motility, which drives tissue dissemination, host cell invasion and egress. A group of plant-like Ca2+-dependent protein kinases (CDPKs), transduce cytosolic Ca2+ flux into enzymatic activity, but the molecular details of their activity are poorly understood. To investigate how Ca2+ signalling activates egress through CDPKs, we performed a forward-genetic screen to isolate gain-of-function mutants from an egress-deficient cdpk3-knockout strain. We recovered mutants that regained the ability to egress from host cells. These harboured mutations in the gene Suppressor of Ca2+-dependent Egress 1 (SCE1). Global phosphoproteomic analysis showed that SCE1 deletion restored many Deltacdpk3-dependent phosphorylation events to near-wild type levels. We also show that phosphorylation of SCE1 is required to relieve its suppressive activity to potentiate egress, and that CDPK3 may regulate this phosphorylation. In summary, our work has uncovered a novel component and suppressor of Ca2+-dependent cell egress during the T. gondii lytic growth.