Therefore, the PPARγ-agonistic potency of lesinurad seems to support its URAT1-inhibitory activity which together form a convenient dual mode of action: while URAT1 inhibition controls uric acid levels and prevents acute inflammatory episodes, PPARγ activation is a validated and efficacious therapeutic approach to metabolic diseases and in addition may particularly reduce the chronic inflammatory aspect of gout. The gene discussed is SLC22A12; the disease is metabolic disease.