A number of studies suggested that crosstalk between HIF-1α and oncogenic c-Myc lead to increased uptake of glucose and its conversion to lactate which subsequently modulate the cancer cell’s microenvironment through regulation of common downstream target genes, such as pyruvate dehydrogenase kinase 1(PDK1) and lactate dehydrogenase A (LDHA)32. The gene discussed is HIF1A; the disease is cancer.