Several studies have suggested that excessively keratinised cells may be responsible for the development of skin lesions in patients with dermatomyositis, in which OAS genes may activate one of the apoptotic cell death mechanisms [38] and resulted that the OAS/RNaseL pathway is a new effector of BRCA1 and IFN-γ-mediated apoptosis [39]. The gene discussed is SMOC1; the disease is dermatomyositis.