BUD23 is an S-adenosyl-L-methionine-dependent methyltransferase that catalyzes N(7)-methylguanosine modification at position 1575 of 18S rRNA, a modification positioned at a functionally important ridge between the P and E tRNA binding sites 1. BUD23 requires the adapter protein TRM112 for full methyltransferase activity and functions in late-stage 40S ribosomal subunit maturation 1. Beyond its catalytic role, BUD23 promotes critical structural transitions in small subunit biogenesis, including central pseudoknot formation, independent of its methylation activity 2. Mechanistically, BUD23 selectively promotes ribosomal interaction with low GC-content 5'UTRs, facilitating efficient translation of specific mRNA transcripts 3. During viral infection, KSHV manipulates BUD23-dependent ribosome biogenesis to generate specialized ribosomes that preferentially translate viral transcripts by reducing ribosome association with upstream open reading frames 4. Clinically, BUD23 overexpression correlates with aggressive malignancies. In hepatocellular carcinoma and kidney renal clear cell carcinoma, elevated BUD23 expression associates with poor survival and reduced immune cell infiltration 56. In prostate cancer, BUD23 upregulation correlates with advanced pathological stages and nodal metastasis, with BUD23 knockdown inhibiting cell proliferation through PPAR signaling modulation 7. BUD23 emerges as essential for cardiac mitochondrial function and embryonic development 3.