Similarly, TOP2A resolves DNA supercoiling to prevent genomic instability; its overexpression in CRC supports proliferation and chemoresistance via pathway modulation.[24–26] In SLE, defective DNA repair exacerbates damage, where TOP2A’s catenation monitoring may falter under oxidative stress, potentially priming colorectal cells for oncogenic mutations.[27,28] Thus, these genes mechanistically link SLE’s immune and DNA repair defects to CRC’s proliferative and invasive traits, highlighting shared inflammatory-genomic pathways. This evidence concerns the gene TOP2A and colorectal carcinoma.