This paper describes the effect of ectopic expression, genetic silencing or pharmacological inhibition of cPLA2α on AKT phosphorylation at Ser473 and cell proliferation in vitro and in vivo of CRC cells with constitutive activation of AKT due to gain-of-function mutations in PI3K, as well as cPLA2α expression and activation in human CRC tissues. Here, AKT1 is linked to colorectal carcinoma.