PTK2 (protein tyrosine kinase 2), also known as focal adhesion kinase (FAK), is a non-receptor tyrosine kinase that regulates cell adhesion, migration, and survival through integrin-mediated signaling 1. PTK2 functions as a key signaling hub downstream of integrin receptors and can be activated by extracellular calcium and stress signals 1. The protein localizes to focal adhesions and regulates actin dynamics through multiple signaling cascades 1. In disease contexts, PTK2 plays critical pathological roles in hepatocellular carcinoma (HCC) progression and metastasis. KLF7-mediated PTK2 upregulation promotes HCC metastasis within an HMGB1-KLF7-TLR4/PTK2 inflammatory axis, with combined PTK2 and TLR4 inhibition showing therapeutic promise 2. Similarly, BACH1 transactivates PTK2 to facilitate HCC growth and metastasis through a positive feedback loop with IGF2/IGF1R signaling; combination therapy targeting both IGF1R and PTK2 suppresses tumor progression 3. Additionally, PTK2 inhibition reduces hepatic stellate cell fibrotic activity and collagen expression in liver fibrosis 4, and suppresses renal tubular epithelial cell pyroptosis in acute kidney injury through integrin β5/FAK signaling 5. In viral pneumonia, PTK2/FAK activation via IFN-γ signaling drives dysplastic cell formation in lung alveoli 6. Recent evidence demonstrates PTK2 negatively regulates ferroptosis in osteoblasts by inhibiting P53 modifications, with PTK2-targeting compounds showing promise for osteoporosis treatment 7.