Finally, in early non-recovery stage of CIN, or initial stage of CKD injury in other words, interstitial capillaries become increasingly permeable allowing that many plasma proteins that never reach the renal interstitium are able to do so and trigger an inflammatory response [25] via the upregulation of NF-κB or MCP-1 [26] and activate oxygen species (ROS) formation [27] leading to glomerulosclerosis. This evidence concerns the gene NFKB1 and cervical squamous intraepithelial neoplasia.