Studies have shown that relying on its c-terminal nuclear localization signal in response to epidermal growth factor, peroxide, growth hormone inhibitor analog TIT-232, IL-3, ultraviolet radiation, and other factors, PKM2 can transfer from the cytoplasm to the nucleus and function as a protein kinase in the dimer form in the nucleus to affect downstream signaling pathways to promote tumor development [15, 35]. Here, GH1 is linked to neoplasm.