Recently, the field has expanded on the types of cisplatin-induced AKI models utilized, the pathomechanism of cisplatin-induced injury unique to reactive oxygen species and mitochondrial dysfunction, pathways of cell death, inflammatory responses, autophagy, and the role of Klotho in AKI [7,8,9,10,11,12,13,14,15,16,17,18,19]. This evidence concerns the gene KL and acute kidney injury.