This will in turn increase PKM2 Ksuc at K311 to inhibit its kinase activity and increase its nuclear translocation by promoting PKM2 tetramer-to-dimer transition, which leads to the interaction of PKM2 with HIF1α and promotes IL-1β transcription and DSS-induced colitis in mice.166 The studies above suggest a key role of protein PTM in linking metabolic reprogramming and inflammation (Fig. 4b). The gene discussed is PKM; the disease is colitis.