On the molecular level, thrombosis in obesity can arise through several pathways, including the effects of adipose tissue-derived cytokines like leptin and adiponectin, enhanced coagulation processes coupled with impaired fibrinolysis, persistent inflammation, oxidative stress leading to endothelial damage, and metabolic disturbances involving lipids and glucose commonly seen in metabolic syndrome (MetS) [4]. This evidence concerns the gene LEP and metabolic syndrome.