The hypothesis that C1qBP could be a Ca2+ chelator/store may explain the earlier observations made by McGee and Baines in which C1qBP was shown to inhibit mPTP activation and that C1qBP overexpression enhanced mitochondria capacity to retain calcium after ROS treatment of MEF cells [9,23], as well as why certain cancer cells overexpress C1qBP as an adaptive response [51–55]; these observations concur with C1qBP acting as a Ca2+ sequester, with cells avoiding Ca2+-induced death amid their elevated calcium-dependent pathways. This evidence concerns the gene C1QBP and cancer.