Moreover, dimeric PKM2 can be maintained by tyrosine phosphorylation34 and other post-translational modifications.35–38 Cancer cells are also particularly adept at re-wiring their metabolism following gene deletion, and indeed PKM1 activity may compensate for the loss of PKM2 in many of the above studies.57,60 No compensatory increase in PKM1 expression was observed in the present study. The gene discussed is PKM; the disease is cancer.