Our mechanistic studies showed that CCL22-activated CCR4 could effectively mediate the membrane recruitment of DGKα via a series of biological events, including mobilization of Ca2+i and activation of PLC-γ1 (an important mediator in Ca2+ signaling pathways), to ultimately phosphorylate a tyrosine residue (Tyr335) in DGKα, after which DGKα interacts with membrane-localized CCR4 in ESCC cells. This evidence concerns the gene CCL22 and esophageal squamous cell carcinoma.