Three mechanisms have been identified that explain the development of this cardiomyopathy, and which can occur in isolation or together causing aggravation; (1) the autoimmune response against the myocardium could be caused by a breakdown of peripheral tolerance that is enhanced by ICI treatment, (2) cross-reactivity of tumor antigens that resemble cardiac or muscle antigens, and (3) elevated blood levels of IL-17a triggered by ICI treatment that have been linked to tissue damage and increased risk of developing ICI-myocarditis. The gene discussed is IL17A; the disease is neoplasm.