Other hypotheses include the suppression of oxidative stress and local inflammation [39] via cyclic adenosine monophosphate (cAMP) and protein kinase A (PKA) mediated inhibition of renal NAD(P)H oxidase [40], the mitigation of oxidative stress-induced autophagy and endothelial dysfunction via downstream restoration of histone deacetylase 6 (HDAC6) facilitated by a GLP-1R-ERK1/2-dependent mechanism [41], and the reduction in circulating angiotensin II levels, which may induce natriuresis by the inhibiting renin-angiotensin system [42]. The gene discussed is FMO5; the disease is endothelial dysfunction.