In the literature, upregulation of activated CaMK2 under hypoxia has been reported in liver cancer but details regarding the isoform CaMK2A were not provided.[38] Apart from calcium‐dependent activation demonstrated by the current work, studies on CaMK2A have shown hypoxia causes oxidation at C280/M281 leading to T286 autophosphorylation and CaMK2A activation in a calcium‐independent manner,[39] suggesting hypoxia might directly activate CaMK2A. Here, CAMK2B is linked to liver cancer.