Collectively, these results add two novel pieces of evidence to our understanding of the molecular underpinnings of SOCE in EPCs: 1) TRPC1 participate to store-dependent Ca2+ inflow in both N-EPCs and RCC-EPCs along with Stim1 and Orai1; and 2) the higher amplitude of SOCE in EPCs isolated from patients suffering from RCC correlates to the over-expression of Stim1, Orai1, and TRPC1. The gene discussed is TRPC1; the disease is renal cell carcinoma.