In tumor cells activated by tyrosine kinase receptor or the KRAS oncogene, AKT(Protein Kinase B, PKB) phosphorylates serine at 90 of PCK1, and phosphorylated PCK1 translocates to the endoplasmic reticulum and loses its original gluconeogenic metabolic enzyme function [20, 28] (Fig. 2). The gene discussed is AKT1; the disease is neoplasm.