In vitro, histidine N-methyltransferase (SETD3) was found to function in regulating the methylation at beta-actin H73, which affected the synthesis of cellular F-actin and the glycolytic phenotype [32], and actin or the actin pathway in chondrocytes was proved to control both skeletal development and associated diseases such as osteoarthritis [33]. The gene discussed is ACTB; the disease is osteoarthritis.