Since ROS overproduction, typically generated by up-regulated Nox, is acknowledged as a key trigger of redox-sensitive pro-inflammatory signaling pathways and oxidative stress-induced insults in atherosclerosis [24,25,26,27], we next investigated the pathophysiological scenario whereby dysregulated LSD1 plays a role in the modulation of Nox subunit gene and protein expression in atherosclerotic mice. This evidence concerns the gene KDM1A and atherosclerosis.