FERMT2 (Kindlin 2) is a scaffolding protein that functions as a critical regulator of integrin activation and cell-matrix adhesion. As an integrin co-activator, FERMT2 enhances integrin-mediated signaling by cooperating with talin proteins and binding to phosphoinositide-enriched membrane regions, facilitating focal adhesion assembly and actin cytoskeleton organization 1. Beyond adhesion, FERMT2 participates in TGFβ signaling pathways and stabilizes β-catenin, influencing Wnt-mediated transcription 2. Clinically, FERMT2 has emerged as a significant disease risk factor across multiple conditions. Genome-wide association studies identified FERMT2 as an Alzheimer's disease (AD) susceptibility gene 3, with functional studies demonstrating that FERMT2 reduction decreases extracellular amyloid-β and phosphorylated tau in human neurons 4. FERMT2 also associates with primary angle-closure glaucoma risk 5. In gastric cancer, FERMT2 drives peritoneal metastasis through anoikis resistance and extracellular matrix remodeling via TGFβ-RI/FN1 signaling, establishing a feedback loop that promotes tumor-stroma crosstalk 26. Similarly, in oral squamous cell carcinoma, FERMT2 upregulation in cancer-associated fibroblasts enhances epithelial-mesenchymal transition and macrophage polarization 7. These findings position FERMT2 as a multi-functional therapeutic target across neurodegenerative and malignant diseases.