The role of previously studied lncRNAs, such as homeobox transcriptional antisense RNA (HOTAIR) and metastasis-associated lung adenocarcinoma (MALAT1), maternally expressed gene 3 (MEG3), taurine upregulated1 (TUG1), and nuclear paraspeckle assembly transcript 1 (NEAT1) (Zhou et al., 2007; Benetatos et al., 2008; Cho et al., 2014; Isin et al., 2014; Handa et al., 2017; Amodio et al., 2018; Dahai et al., 2019; Taiana et al., 2019; Shehata et al., 2020), have been widely accepted for their biological functions and mechanisms in the development of MM. This evidence concerns the gene MALAT1 and Miyoshi myopathy.