AKT1 and in situ carcinoma: In terms of UBUC, low-grade disease (~80%) is featured by hyperplasia, papillary phenotype, fibroblast growth factor receptor 3 (FGFR3) mutations, HRAS mutations, activation of the phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA)/AKT/mTOR pathway, and better outcomes, while high-grade disease (~20%) is characterized by dysplasia, carcinoma in situ, p53 loss, Rb loss, and worse outcomes (36).