In contrast, HDAC6-specific inhibition through the HDACis tubacin, tubastatin A and ST-80 across a panel of urothelial cancer-cell lines, including bladder cancer ones, revealed only moderate efficacies in the induction of cell-cycle arrest or cell viability reduction, and exerted only minor effects on migration and invasion, hence suggesting that growth and survival of urothelial cancer cells may not critically depend on HDAC6 function [174]. This evidence concerns the gene HDAC6 and urinary bladder carcinoma.