ITGBL1 encodes an extracellular matrix protein that functions as an integrin-binding molecule involved in cell adhesion, migration, and focal adhesion formation. The gene promotes integrin-mediated signaling and is expressed at the cell surface and in plasma membrane-associated structures. In cancer contexts, ITGBL1 drives metastatic progression through multiple mechanisms. In gastric cancer, ITGBL1 overexpression enhances anoikis resistance and metastatic potential via the AKT/FBLN2 signaling axis, with elevated expression correlating with poor prognosis 1. In colorectal cancer, primary tumors release ITGBL1-enriched extracellular vesicles that activate resident fibroblasts in distant organs through TNFAIP3-mediated NF-κB signaling, establishing a pre-metastatic niche that promotes metastatic growth 2. ITGBL1 also promotes castration-resistant prostate cancer progression through cancer-associated fibroblasts via the AR/ITGBL1 axis 3. Outside oncology, ITGBL1 participates in fibrotic pathways. In chr13 hepatitis B, HBV infection upregulates ITGBL1 through the RUNX2 transcription factor, driving hepatic stellate cell activation and liver fibrosis progression 4. In wound healing, ITGBL1-expressing fibroblasts promote scarring and fibrogenesis; mechanical pressure therapy reduces ITGBL1 expression via the SMYD3 pathway, inhibiting myofibroblast progression and scarring 5. In acute myeloid leukemia, ITGBL1 hypermethylation is an independent prognostic factor associated with poor overall survival and treatment resistance 6.