KLRG1 and neoplasm: Finally, although bladder cancer can downregulate E-cadherin during epithelial-mesenchymal transition, pathologic series have confirmed that up to half of high-grade/invasive urothelial carcinomas still retain E-cadherin protein expression, and our own flow cytometry confirms retention of E-cadherin in a proportion of tumor cells (Figure 7C), indicating that urothelial carcinoma can still initiate KLRG1-dependent inhibition.