As CKD is in a chronic inflammatory state, mitochondrial dysfunction, cellular damage and apoptosis in damaged cells induce an increase in ROS production and exceed the antioxidant defences, leading to ROS accumulation in the body, triggering a downstream inflammatory cascade [62], activating the transcription factors NF-κB, AP-1, and p53, and promoting pro-inflammatory cytokine and chemokine production [63–65], further exacerbating the inflammatory state and promoting the disease progression of CKD [66] and renal fibrosis [67]. This evidence concerns the gene TP53 and chronic kidney disease.