CLIP1 (CAP-Gly domain containing linker protein 1) is a microtubule plus-end binding protein that regulates microtubule dynamics and intracellular trafficking. Primary functions include promoting microtubule growth and bundling, linking cytoplasmic vesicles to microtubules for transport, and regulating macropinocytosis and endosome trafficking. CLIP1 possesses RNA-binding activity with specificity for UGGGGAGG motifs 1. Mechanistically, CLIP1 modulates inflammatory signaling by regulating TIRAP ubiquitination and degradation through interaction with TFPI2, thereby suppressing TLR4/NF-κB-mediated responses 2. Clinically, CLIP1 alterations are implicated in multiple cancers. CLIP1-LTK fusion represents a novel oncogenic driver in 0.4% of non-small-cell lung adenocarcinomas, demonstrating constitutively activated kinase activity responsive to ALK inhibitor lorlatinib treatment 3. CLIP1-RAF1 fusion is a recurrent driver event in infantile fibrosarcomas, promoting cell proliferation and migration through constitutive MAPK and PI3K-AKT pathway activation 4. Additionally, CLIP1 mutations are associated with vascular invasion in poorly differentiated thyroid cancer 5, and reduced CLIP1 expression serves as a potential biomarker in prostate cancer 6. Notably, CLIP1 loss-of-function mutations cause autosomal recessive intellectual disability, highlighting its essential role in neuronal development and axonal transport 7.