SYNCRIP (hnRNP Q) is a heterogeneous nuclear ribonucleoprotein that functions as a multifaceted post-transcriptional regulator. Primary functions include mRNA processing and stability control; it associates with pre-mRNA and mature mRNA complexes 1 and is a component of the CRD-mediated mRNA stability complex that promotes MYC mRNA stability. SYNCRIP modulates APOB mRNA C-to-U RNA editing and participates in the GAIT complex, which selectively suppresses translation of inflammatory mRNAs upon interferon-gamma activation 2. Mechanistically, SYNCRIP regulates cortical neurogenesis by maintaining transcription factor expression through phase-separation-dependent complex formation, crucially controlling the Notch signaling pathway that determines radial glial cell fate 3. It also interacts with LIN28B to modulate the LIN28B/let-7 tumor-suppressive axis in hepatocellular carcinoma 2. Disease relevance spans neurodevelopmental and cancer contexts. Rare deleterious SYNCRIP mutations contribute to neurodevelopmental disorders with enriched de novo variants 1, and SYNCRIP knockout disrupts cortical layer development and causes learning impairments in mice 3. In cancer, SYNCRIP loss unleashes APOBEC3B-driven mutagenesis and therapy resistance in prostate cancer 4, while elevated SYNCRIP promotes colorectal cancer proliferation via DNMT3A/p16 dysregulation 5. High SYNCRIP expression predicts poor outcomes in hepatocellular carcinoma and ovarian cancer 26, and its secretion from treated ovarian cancer cells enhances therapy resistance 7.