Whereas traditional models treat psychosocial stress as a contextual factor, our model emphasizes its role as a biological amplifier of lipid-driven atherothrombosis—through neuroendocrine activation, NLRP3 inflammasome signaling, oxidative stress, and endothelial dysfunction [19,20,21,22,23,24]. The gene discussed is NLRP3; the disease is endothelial dysfunction.