Although the mechanism of DM is largely unknown, some factors are thought to contribute to DM pathogenesis, such as MHC polymorphisms, epigenetic modifications, type I interferon (IFN) signalling, myositis-specific antibodies and many other pathways, such as the phosphoinositol-3-kinase (PI3K)–v-akt murine thymoma viral oncogene homologue (Akt), mitogen-activated protein kinase (MAPK), adenosine monophosphate-activated protein kinase (AMPK) and Forkhead box O (FoxO) signalling pathways (Lahoria et al., 2016; Gao et al., 2017; Tartar et al., 2018; Gao et al., 2019). The gene discussed is HLA-C; the disease is dermatomyositis.