KRT72 and neoplasm: We observed a number of abnormalities in Pparg mutants that are similar to those observed in MIBC subtypes with low Pparg expression, including increased expression of basal/squamous markers (Krt14, Krt6, Krt5), persistent NF-κB signaling25,51, and up-regulation of pathways activated during invasion (Snail1, Slug, and vimentin) as well as a compromised basement membrane (Fig. 9). Despite these similarities, we did not observe tumor formation in ShhCre;Ppargfl/fl mutants, suggesting that Pparg mutations are unlikely to be primary drivers of tumor formation.