Our data suggest that HIF-1α and PKM2 are both essential downstream factors for HITT's inhibition of tumorigenesis, while the proportional contribution of HIF-1α and PKM2 to HITT-mediated tumor suppression in vivo needs to be evaluated in future studies, and whether HITT may bind with additional glycolysis regulators under different conditions warrants further investigation. This evidence concerns the gene PKM and neoplasm.