Additionally, multiple recent studies investigating the relationship between SGLT2 inhibitors and complement suggest that empagliflozin and dapagliflozin attenuate and mediate complement-influenced disease processes in murine models of kidney disease, which holds intriguing implications for empagliflozin as a possible treatment agent in PAH [190,191]. The gene discussed is SLC5A2; the disease is pulmonary arterial hypertension.