Similarly, when tumor cells are exposed to stress or anti-chemotherapeutic drugs, such as increased expression of hypoxia inducible factor-1α (HIF-1α) in cells during hypoxia, both the transcriptional activity of PKM2 and the proportion of tetrameric PKM2 can be increased, similarly when cisplatin etc. using ROS as a killing chemotherapeutic agent that acts on tumor cells is used [52], PKM2 reforms into a tetrameric form, open the tricarboxylic acid cycle (TCA) and the electron transport chain to consume excess reactive oxygen species in the cell and protect the mitochondria from drug attack. The gene discussed is PKM; the disease is neoplasm.