Several studies have identified pathophysiologic links between SARS-CoV-2 and IIMs, including shared immunoglobulin epitope signatures between anti-transcription intermediary factor 1 (TIF1)-γ-positive dermatomyositis patients and SARS-CoV-2 [2] as well as similarities between SARS-CoV-2 infection and positive anti-melanoma differentiation-associated protein 5 (MDA5) dermatomyositis which may be suggestive of a shared pathogenic link [4]. The gene discussed is TRIM33; the disease is dermatomyositis.