The abundant IFN further upregulates cytoplasmic MDA5 expression,[10,11] potentially inducing autoimmune responses.[12] Recent evidence demonstrates increased IFN-1 expression in alveolar epithelial cells of MDA5-positive DM patients.[13] Transcriptomic analyses suggest a central role for the type I IFN pathway in MDA5 + DM pathogenesis, with RPILD patients exhibiting significantly elevated serum IFN-γ levels and strong IFN-γ-related immune responses in lung tissue and hilar lymph nodes.[14]. This evidence concerns the gene IFNG and dermatomyositis.