Moreover, inactivation of STAG2, unlike other cohesin complex proteins, was previously reported to only have no to minimal effects on TADs in MCF10A human transformed breast epithelial cells12, mouse embryonic stem cells16, mouse HSPCs11, HCT116 human colorectal carcinoma cells32, or RT112 bladder cancer cells39, which led to the hypothesis that STAG2 may not be required for the maintenance of TADs, probably due to compensation of STAG12. This evidence concerns the gene STAG2 and urinary bladder carcinoma.