Nuclear translocation of dimeric PKM2 is promoted both by tumor-specific characteristics and tumor microenvironment such as excessive EGFR activation and hypoxia.[10,20] To illustrate, EGFR activation leads to ERK2-PKM2 binding and phosphorylation of PKM2 at S37, which facilitates PIN1-mediated cis-trans isomerization of PKM2. The gene discussed is EGFR; the disease is neoplasm.