A plausible explanation is that alterations of ORAI1/ORAI3 ratio,[34] or changes in expression ratios of ORAI/STIM variants,[7] may disrupt the dynamic equilibrium of SOC channels that function as pro‐oncogenic switches in certain types of cancer.[35] It is likely that augmented STIM1β expression could lead to a similar scenario via heterotypic interactions with other STIM/ORAI proteins. Here, UBXN11 is linked to cancer.