EGFR inhibition decreases T cell proliferation, activation, and cytokine production, leading to reduced T cell infiltration in atherosclerotic lesions.594 Additionally, IL-35 promotes the survival of reparative CX3CR1+Ly6Clow macrophages, which in turn reduces cardiac rupture, improves wound healing, and attenuates cardiac remodeling after MI by enhancing α-SMA and collagen expression.595 Thrombospondin-1 (TSP1), a well-known inhibitor of angiogenesis, exerts its effects by interacting with cell surface receptors such as CD36 and CD47. Here, EGFR is linked to myocardial infarction.