ZNF593 is a zinc finger protein with multiple regulatory functions spanning nuclear and cytoplasmic compartments. Structurally, it comprises a classic C(2)H(2) zinc finger domain flanked by disordered regions 1. Nuclearly, ZNF593 negatively modulates Oct-2 transcriptional activity by inhibiting its DNA binding 2, and interacts with ZFX to facilitate histone H4 acetylation and transcriptional elongation 3. Additionally, ZNF593 promotes pre-60S ribosomal particle nuclear export during ribosomal maturation. In the cytoplasm, ZNF593 functions as a critical immune checkpoint. Following viral infection, ZNF593 translocates from the nucleus to the cytoplasm where it directly binds cGAS and suppresses its DNA-binding capacity, thereby attenuating the cGAS-mediated antiviral interferon-β response 4. ZNF593 deficiency enhances antiviral immunity and improves survival against HSV-1 infection. Clinically, ZNF593 dysregulation is implicated in systemic lupus erythematosus pathogenesis; restoring ZNF593 expression reduces pathogenic interferon production in SLE patients and animal models 4. Beyond immunity, ZNF593-AS (an antisense transcript) protects against cardiac hypertrophy by upregulating mitofusin-2 and improving mitochondrial function 5. These findings establish ZNF593 as a multifunctional regulator bridging transcription, ribosomal biogenesis, and innate immunity.