Moreover, TRPC6 is upregulated in several proteinuric kidney diseases including DN [19–21], which may be relevant to podocyte damage because Angiotensin II, reactive oxygen species (ROS), and other factors in the setting of DN directly activate TRPC6 activity and result in drastic increases in Ca2+ influx, causing podocyte actin cytoskeleton dynamics, hypertrophy, and foot process effacement [22–25]. The gene discussed is AGT; the disease is liver dysplastic nodule.