CELF2 is an RNA-binding protein that regulates post-transcriptional gene expression through multiple mechanisms. Functionally, CELF2 modulates alternative pre-mRNA splicing, mRNA stability, and translation by binding to UG-rich and AU-rich sequence motifs 1. It specifically regulates tissue-specific splicing events, including TNNT2 exon 5 inclusion in embryonic muscle and smooth muscle-specific actinin exon inclusion [UniProt]. CELF2 also negatively regulates miRNA biogenesis by binding pri-MIR140 [UniProt]. CLINICALLY, CELF2 dysregulation is implicated in multiple disease contexts. Loss of CELF2 promotes acute myeloid leukemia development by stabilizing FAT10 mRNA and activating mTORC1 signaling 2. Conversely, CELF2 acts as a tumor suppressor in bladder cancer by decreasing CXCL5 mRNA stability 3 and in colorectal cancer by inducing autophagy-mediated cell death 4. CELF2 is downregulated in various cancers and associated with poor prognosis 5. Additionally, CELF2 mutations cause neurodevelopmental disorders; heterozygous CELF2 variants are linked to developmental and epileptic encephalopathy 6, and Celf2 deficiency in mice produces autism-like behaviors with impaired dendritic spine and synapse development 7. CELF2 overexpression may also benefit diabetes-induced erectile dysfunction through enhanced angiogenesis 8.