Importantly, Akt can directly phosphorylate PFKP at S386, which prevents the interaction of PFKP with E3 ligase TRIM21 and the subsequent TRIM21-mediated polyubiquitination and degradation of PFKP, resulting in increased PFKP expression, aerobic glycolysis, cell proliferation, and tumor growth (Lee et al., 2017). This evidence concerns the gene AKT1 and neoplasm.