This concept was reinforced by results from in vitro, in vivo, and clinical endocrinology studies proposing that mechanisms involving gut dysbiosis, renal nicotinamide adenine dinucleotide phosphate oxidase 4, nuclear factor erythroid 2-related factor 2, endoplasmic reticulum stress, and the NOD-like receptor protein 3 inflammasome may represent key molecular targets through which anthocyanins mitigate uric-acid-induced kidney injury [49]. Here, NFE2L2 is linked to kidney injury.