Experimental studies have shown that hyperuricaemia leads to elevated levels of systemic inflammatory factors and may also have the ability to induce systemic inflammation via the NF-kB signaling pathway, and that UA induces inflammation via the AMP-activated protein kinase-mTOR (mammalian target of rapamycin) mitochondrial ROS and hypoxia-inducible factor-1α pathways (Zhang et al., 2023). This evidence concerns the gene NFKB1 and hyperuricemia.