For further verification, by transfecting wild-type or mutant LATS1 plasmids into 293T or bladder cancer cells and confirmed that mutation of SBC1 led to remarkable blockade of LATS1 degradation mediated by SPOP, while depletion of SBC2 had little effect (Fig. 3m and Fig. S5b). The gene discussed is LATS1; the disease is urinary bladder cancer.