Furthermore, research has revealed that T lymphocytes contribute to the development of DCM through direct cytotoxic effects, activation of other immune cells, and support of pathogenic antibody production by B cells [94] Particularly, CD4+ T cells have been identified as a major contributor to cardiac fibrosis, primarily through pro-inflammatory Th1 and Th17 subsets and their associated cytokines, such as IL-6, IL-1β, TNF, and IL-17, which can activate resident cardiac fibroblasts and promote fibrosis [95,96,97]. The gene discussed is IL1B; the disease is familial dilated cardiomyopathy.