Our study confirmed that the decreased expression level of mitochondrial fusion genes (OPA1, MFN2) and the increased expression level of mitochondrial division genes (Drp1, Fis1) in patients with coal workers' pneumoconiosis suggested that the number of short mitochondria increased, and the repair ability of damaged mitochondria decreased, resulting in cellular dysfunction. The gene discussed is MFN2; the disease is pneumoconiosis.