This may be due to the fact that visceral fat, as an ‘endocrine organ’, releases a large amount of free fatty acids (FFA), pro-inflammatory cytokines (such as interleukin-6, tumour necrosis factor-α, and leptin), and pro-thrombotic factors, amplifying the already existing inflammatory response in sepsis, inducing insulin resistance and lipid metabolism disorders, and promoting endothelial dysfunction and a hypercoagulable state [33–35]. The gene discussed is LEP; the disease is Sepsis.