The data showed us key members of the cell stress response pathway, including epidermal growth factor receptor (EGFR), mitogen-activate protein kinase 3 (MAPK3), nuclear factor kappa B subunit 2 (NFKB2) and so on (Fig. 7c, red outer circles), interacted with wild-type TKT but not with the NLS mutant, suggesting potential non-metabolic mechanisms of nuclear TKT for promoting the development of HCC. This evidence concerns the gene MAP4K3 and hepatocellular carcinoma.