AKT1 and hepatocellular carcinoma: In vitro, they found that activation of PKM2 in the HCC cell line HLE transfected with Akt and dominant negative Spry2 is independent of ERK and AKT cascades, collectively implying that loss of Spry2 synergizes with activated AKT to induce rapid hepatocarcinogenesis through the activation of ERK and PKM2 pathways.