In late stages of atherosclerosis, when apoptosis is either overwhelmed or inhibited, foam cells can undergo necroptosis through the receptor-interacting serine/threonine-protein kinase 1 (RIPK1), RIPK3, and mixed-lineage kinase domain–like pseudokinase (MLKL) cascade, resulting in the bursting of the cellular membrane and release of its inflammatory content (48, 49). Here, RIPK1 is linked to atherosclerosis.