ORAI1 and neoplasm: have proposed that, during carcinogenesis, colorectal cancer cells may switch from a small, transient SOCE based on ORAI1-dependent CRAC channels (normal cells) to large and sustained currents depending on both ORAI1 and TRPC1 channels (tumor cells) (Villalobos et al., 2016; Villalobos et al., 2017; Villalobos et al., 2019).