Whereas the CKα isozyme has become a target for interference with phospholipid metabolism in anticancer strategies, the pronounced alteration of CKβ catalytic activity and inhibition by HC-3 observed after PKA phosphorylation strongly suggests that this isoform could also be implicated in carcinogenesis and be considered as potential target for anti-choline kinase drugs, especially in liver and thymus tumors that do not overexpress CKα [45]. Here, CKB is linked to thymus neoplasm.