ZNF93 is a primate-specific KRAB zinc finger transcription repressor that primarily functions to silence retrotransposons, particularly L1 elements 1. ZNF93 recognizes and binds specific L1 sequences (L1PA3-L1PA6 subtypes) and recruits the TRIM28/KAP1 co-repressor complex to repress their transcription 1, with structural studies confirming the critical KRAB-KAP1 molecular interface required for this repressive activity 2. However, ZNF93 exhibits selective restriction; approximately 50% of L1PA3 elements have lost its binding site, and it does not repress the most recently evolved L1PA2 and L1Hs subtypes, demonstrating an evolutionary arms race between this zinc finger protein and retrotransposons 1. Beyond retrotransposon silencing, emerging evidence reveals ZNF93's broader oncogenic roles. It regulates APOBEC3B expression, a mutagenic enzyme implicated in tumorigenesis, and its overexpression correlates with enhanced resistance to genotoxic stress and genomic instability 3. In cancer contexts, ZNF93 promotes tumor cell proliferation through transcriptional regulation of oncogenes like PRPF3 in hepatocellular carcinoma 4, while its overexpression confers resistance to therapeutic agents including trabectedin, zalypsis, and cisplatin 5. Rare ZNF93 variants show association with lung cancer susceptibility 6.