For example, in human colon cancer, a complex interplay between TRPC1/Orai1 and STIM2 was identified, with TRPC1/Orai1 expression upregulation being associated with increased SOCE and Ca2+ store content, whereas STIM2 downregulation underlying Ca2+ store depletion and promoting apoptosis resistance [191]. This evidence concerns the gene TRPC1 and colonic neoplasm.