The proposed pathophysiological mechanisms include systemic inflammation, endotoxaemia, and haemodynamic instability, which collectively suppress ACTH secretion, impair adrenal steroidogenesis, and reduce adrenal perfusion [8]. In decompensated cirrhosis, adrenal dysfunction is influenced by several disease-specific factors, including reduced cholesterol substrate, impaired cortisol biosynthesis, attenuated responsiveness to ACTH, and lower circulating levels of cortisol-binding proteins such as CBG and albumin. The gene discussed is ALB; the disease is Cirrhosis.