The literature demonstrates that sorafenib, by inhibiting targets such as VEGFR and PDGFR, disrupts endothelial cell function and vascular homeostasis, potentially leading to coronary artery spasm or atherosclerosis, which may subsequently trigger acute coronary syndromes (e.g., ST-segment elevation myocardial infarction) (13–15). This evidence concerns the gene KDR and acute coronary syndrome.