Our previous study found that EBV infection can activate epidermal growth factor (EGF)-induced, SOCE-mediated Ca2+ signaling and increase VEGF production to promote NPC tumor angiogenesis [12] and blocking SOCE using SKF96365 or 2-aminoethoxydiphenyl borate can inhibit the growth and angiogenesis of NPC [12,13]. The gene discussed is VEGFA; the disease is Epstein-Barr virus infection.