These molecules interact with the receptors (e.g., integrin αvβ5, MERTK, transglutaminase 2, low-density lipoprotein receptor-related protein 1 [LRP1], and scavenger receptor B) on phagocytes via bridging molecules, resulting in the activation of enzymes involved in phagolysosomal degradation and efferocytosis during early lesion formation.19, 20, 21, 22 Efferocytosis also limits the progression of atherosclerosis via indirectly inhibiting the generation of reactive oxygen species (ROS) and pro-inflammatory mediators, and directly enhancing anti-inflammatory and anti-oxidant responses.23 The gene discussed is LRP1; the disease is atherosclerosis.