CAMK2G and neoplasm: Sev may disrupt Ca2+ homeostasis by elevating Ca2+ concentration, leading to endoplasmic reticulum stress, which ultimately activates CaMKII and stimulates the phosphorylation of CaMKII and c-Jun N-terminal kinase (JNK) in a dose-dependent manner, inhibiting tumor growth and the stemness of GSCs both in vitro and in vivo.