In addition, decreased staining of Ki-67, CDH4, and β-catenin, and increased staining of cleaved caspase-3 were observed after ALKBH5 depletion, which was abrogated by lncRNA SNHG15 overexpression, indicating that ALKBH5-lncRNA SNHG15 axis modulates in vivo MM biological function via modulating SETD2/H3K36me3 and thus CDH4/β-catenin. The gene discussed is MKI67; the disease is Miyoshi myopathy.