ABCG2, localized on the basolateral membrane, plays a pivotal role in maintaining the balance between urate secretion and reabsorption and is closely linked to the pathogenesis of hyperuricemia.[32] Damage to renal tubular epithelial cells is a critical factor in urate‐induced kidney injury.[33] Studies have demonstrated that IL‐1β can suppress ABCG2 expression by downregulating the PDZK1 protein.[34] Therefore, the regulatory mechanism of curcumin on ABCG2 protein expression may involve the inhibition of IL‐1β release, thereby promoting the activation of ABCG2. The gene discussed is IL1B; the disease is hyperuricemia.