Similarly, Erbel et al. (16) reported that inhibiting IL-17A in ApoE−/− mice slowed the progression of advanced atherosclerotic lesions by reducing the necrotic core of atherosclerosis and that IL-17A mAb treatment slowed the progression of advanced atherosclerotic lesions by increasing fibrous cap thickness, collagen content, and connective tissue growth factor (CTGF) mRNA expression to exert a plaque-stabilizing effect. Here, IL17A is linked to atherosclerosis.