CDKN2A and fibrosis: This study demonstrated that impaired renal structure including thinner renal cortex and decreased glomeruli, dysfunction, decreased renal cell proliferation, increased renal cell apoptosis, senescence and SASP with DNA damage, NF-kB-p65 and TGF-β1/Smad signal activation, inflammatory cell infiltration, tubulointerstitial fibrosis and tubular atrophy caused by Bmi-1 deficiency were largely rescued by p16 deletion.