Beginning with the decreased availability of GLUT 1/4 and HK1, which catalyze the rate‐limiting and first necessary step of glucose metabolism, as well as the multifunctional PGI and PFKM, the juvenile myocardium's glycolysis appears to be dysregulated in MetS at the protein level, mRNA level, and availability in glycolysis metabolic intermediates. The gene discussed is PFKM; the disease is metabolic syndrome.