We previously demonstrated that the levels of key glycolytic enzymes, including hexokinase2 (HK2), pyruvate kinase M2 (PKM2), lactate dehydrogenase A (LDHA), and the lactate concentration were enhanced in silica-induced alveolar macrophage and silicotic models, suggesting that the metabolic switch to glycolysis is an important driving force for the development of silicosis fibrosis [4]. The gene discussed is LDHA; the disease is silicosis.