Additionally, the genetic deletion of CXCL4 has been shown to decrease atherosclerosis (37) and exogenous CXCL4 has been observed to diminish the phagocytic capacities of macrophages involved in myocardial infarction by reducing the expression of CD36, a dual receptor involved in both the engulfment of apoptotic cells and the uptake of modified lipids (23). This evidence concerns the gene PF4 and myocardial infarction.