As insulin resistance and hyperglycemia are linked to the development of clinically significant unstable atherosclerotic plaques [22], and activated MK2 in lesional macrophages can impair efferocytosis and resolution [11, 12], we hypothesized that MK2 could represent a promising therapeutic target to prevent unstable plaque formation in the setting of insulin resistance. The gene discussed is MAPKAPK2; the disease is Insulin resistance.