For example, first, in principal cells of the cortical collecting duct, spironolactone attenuated aldosterone-induced inflammatory cytokines production such as IL-1β and IL-6 via mineralocorticoid receptor-dependent pathway [43], second, in human mononuclear cells, spironolactone inhibited the activation of NF-κβ and the expression of several NF-κβ-targeted genes via non-mineralocorticoid receptor mechanisms [44], [45], third, in rheumatoid arthritis patients, treatment with spironolactone improves both endothelial dysfunction and inflammatory disease activity [24], [27]. Here, NFKB1 is linked to endothelial dysfunction.