Pharmacological activation of PPARβ/δ has been shown to reduce hypertension, endothelial dysfunction, and organ damage in mice with severe lupus, which was associated with reduced plasmatic anti-dsDNA autoantibodies and anti-inflammatory and antioxidant effects in target tissues, identifying PPARβ/δ as a promising target for an alternative approach to the treatment of SLE and its associated vascular damage [17]. The gene discussed is PPARD; the disease is systemic lupus erythematosus.