The c-MYC-induced upregulation of relevant glycolytic enzymes such as Glucose Transporter 1 (GLUT1) and Lactate Dehydrogenase A (LDHA) [6, 7] results in an enhanced uptake and conversion of glucose into the oncometabolite pyruvate followed by a LDHA mediated increase in lactic acid and acidification of the tumor microenvironment (TME) [8]. The gene discussed is LDHA; the disease is neoplasm.