CSNK2A1 encodes the catalytic alpha subunit of casein kinase 2 (CK2), a constitutively active serine/threonine kinase that phosphorylates substrates with acidic residues at the C-terminus. The protein regulates diverse cellular processes including cell cycle progression, apoptosis, transcription, and DNA damage response. During mitosis, CK2 maintains the p53-dependent spindle assembly checkpoint and G2 arrest upon spindle damage. In response to DNA damage, CK2 phosphorylates repair proteins such as MDC1, MRE11, RAD51, and RAD9A, promoting their recruitment to damage sites. CK2 also suppresses apoptosis by phosphorylating caspases and protective factors, while supporting transcription through direct phosphorylation of RNA polymerases and transcription factors including NF-κB, STAT1, and MYC. Recent evidence suggests CK2 negatively regulates autophagy by activating TRIM proteins, with pharmacological inhibition promoting autophagy-dependent restriction of viral infections 1. De novo mutations in CSNK2A1 are enriched in developmental disorders, where they cause Okur-Chung neurodevelopmental syndrome (OCNDS), presenting with developmental delay, intellectual disability, autism, speech delays, and epilepsy in approximately 25% of cases 2. In cancer, CSNK2A1 is frequently upregulated and associated with poor prognosis in hepatocellular carcinoma and colorectal cancer, where it promotes epithelial-mesenchymal transition and activates growth-promoting pathways such as PI3K-AKT-mTOR 3, 4. Mutations in CSNK2A1 have also been identified in adult T cell leukemia/lymphoma 5. The kinase inhibitor silmitasertib and small-molecule CK2 inhibitors such as CX-4945 and emodin show promise in suppressing cancer cell proliferation and chemoresistance 6, 7.