A possible mechanism may be that glucose phosphorylation and HK-II binding to the mitochondrial membrane were increased, which inhibited cytochrome C release and apoptosis and reduced glucose-6-phosphate negative feedback on glycolysis; this may have increased glycolysis and substrate product biosynthesis, increasing the growth of cancer cells and acidulating the cancer microenvironment to promote tumor invasion [114]. The gene discussed is CYCS; the disease is cancer.