This is the case for anti–TIF1-γ–positive dermatomyositis (DM) patients, who typically present with clinical erythroderma and extensive psoriasiform and hyperkeratotic plaques, as well as for anti–MDA5–positive DM patients, who often develop necrotic cutaneous ulcers, telangiectasias, poikiloderma, and diffuse interstitial lung disease (ILD). The gene discussed is TRIM33; the disease is dermatomyositis.