For example, inhibition of choline metabolism by CHKα inhibitors or genetic silencing of CHKα by siRNA results in reduced PI3K-mTOR-Akt, Ras-Raf-MAPK-AP1 or EGFR-mTorc2 signaling in different cancer models, highlighting a causal role of CHKα elevation in carcinogenesis and tumor progression [1,3,15]. This evidence concerns the gene CHKA and neoplasm.