The possible mechanisms responsible for the increased mortality associated with BsmI polymorphism in hemodialysis patients are as follows: modification of vitamin D receptor sensitivity and expression in cardiac and vascular tissues, modification of the circulating levels of vitamin D due to the influence of vitamin D receptors on the feedback mechanism for the regulation of alpha-1-hydroxylase, hyperparathyroidism with calcium-phosphate imbalance, which predisposes to cardiac and vascular calcifications, and hampered calcitriol effects [130]. The gene discussed is VDR; the disease is hyperparathyroidism.