Fibrosis is the histologic hallmark common to all CKD models, and hence, we analyzed the bulk RNA-seq data from three mouse models for renal fibrosis: unilateral ureteric obstruction induced by surgical ligation of the ureter (UUO, Arvaniti et al.10), toxic precipitation in the tubules induced by high dose folic acid injection (FA, Craciun et al.11), or genetic alteration by transgenic expression of genetic risk variant APOL1 in podocytes (APOL1 transgenic mice12). This evidence concerns the gene APOL1 and chronic kidney disease.