In bladder cancer cell lines, silencing TM4SF1 activated the PPARγ-SIRT1 feedback loop, promoting the formation of ROS and increasing the expression of SOD2 and catalase 8, revealing that excess ROS were produced by disrupting homeostasis, resulting in oxidative stress and death in bladder cancer cells 81. This evidence concerns the gene TM4SF1 and urinary bladder carcinoma.