However, Gu et al. provided the possible involvement of p38 in M2 macrophage polarization under the development of lung fibrosis, focusing on mitochondrial calcium uniporter (MCU)-mediated fatty acid oxidation (FAO) in macrophages: (1) MCU expression polarized macrophages to a profibrotic phenotype during asbestos-induced lung fibrogenesis. The gene discussed is MAPK14; the disease is pulmonary fibrosis.