PTK2, also known as focal adhesion kinase (FAK), is a cytoplasmic protein tyrosine kinase. It is crucial in various biological processes, such as cell movement, invasion, survival, gene expression, and cancer stem cell self-renewal, and is involved in multiple signaling pathways [3].

In hepatocellular carcinoma (HCC), genetic depletion of KLF7, which upregulates PTK2, impedes HMGB1-mediated HCC progression and metastasis, indicating PTK2's role in promoting HCC metastasis [1]. In IPF, PTK2 levels are higher in lung tissues of patients, and a PTK2-associated gene signature can predict prognosis, suggesting its potential as a molecular target and prognostic biomarker [2]. In HCC, PTK2 promotes cancer stem cell traits by activating Wnt/β-catenin signaling, leading to HCC recurrence and sorafenib resistance [4]. Also, in HCC, the combination of IGF1R inhibitor and PTK2 inhibitor defactinib suppresses BACH1-mediated HCC growth and metastasis, highlighting PTK2's role in HCC growth and metastasis [5]. In another study on HCC, the combination of PTK2 inhibitor defactinib and c-MET inhibitor capmatinib significantly suppressed HCC metastasis induced by ETV1, which upregulates PTK2 [6].

In conclusion, PTK2 is a key cytoplasmic protein tyrosine kinase involved in various biological processes. Through gene-knockout or related functional studies in disease models like HCC and IPF, it has been revealed that PTK2 plays important roles in tumor progression, metastasis, and may serve as a potential therapeutic target and prognostic biomarker in these diseases.