FERMT3 encodes kindlin-3, a focal adhesion protein that functions as a critical regulator of integrin activation in leukocytes and platelets 1. The protein mediates cell-substrate and cell-cell adhesion through integrin-dependent signaling pathways 2, playing essential roles in leukocyte trafficking, platelet aggregation, and endothelial barrier function 3. At the molecular level, kindlin-3 facilitates liquid-liquid phase separation required for focal adhesion assembly and maturation; under oscillatory shear stress, arginine methylation of kindlin-3 impairs this process, compromising vascular stability 3. Losses of FERMT3 function cause leukocyte adhesion deficiency-III (LAD-III), a rare autosomal recessive syndrome characterized by defective leukocyte activation, integrin dysfunction, and combined bleeding and immune defects 4. Beyond infectious immunity, FERMT3 emerges as a prognostic biomarker in multiple diseases: it associates with immune infiltration and improved anti-PD1 immunotherapy response in glioma 5, correlates with kidney disease progression in ADPKD 6, and links to inflammatory severity in sepsis and ankylosing spondylitis 72. FERMT3 participates in inherited platelet dysfunction syndromes alongside integrin defects 8, highlighting its importance for hemostasis and immune cell adhesion pathways.