As another possible mechanism for defective efferocytosis, the pro-inflammatory molecule high-mobility group box 1 (HMGB1) is increased in human and murine atherosclerosis (83, 84), and the secreted form has been shown to interact with integrin αVβ3 and PtdSer to block efferocytosis (85, 86). This evidence concerns the gene HMGB1 and atherosclerosis.