These reactions are enhanced in uremia where there is increased concentration of many α-oxaldehydes such as glyoxal, methylglyoxal etc. Like AOPPs, AGEs are also a class of uremic toxins.[33–35] ROS may disrupt copper binding to CP, thereby impairing its normal protective function while liberating the copper.[36] Thus, formation of uremic toxins and damage due to ROS may decrease CP levels in CRF patients. The gene discussed is CP; the disease is uremia.