With this hypothesis in mind, we performed pilot studies of a mouse model of IC/PBS based on inhibition of bladder epithelial repair by synthetic as-APF, using acetic acid to induce epithelial damage as previously described for a rabbit model of cystitis as well as a rat model of colitis [49,50], and determining bladder epithelial area, UPIII and ZO-1 gene expression (all previously shown to be abnormally decreased in IC/PBS patient biopsy specimens). The gene discussed is UPK3A; the disease is chronic cystitis.