While focal adhesion kinase (FAK) hyperactivation in human pancreatic ductal adenocarcinoma (PDAC) was found to be associated with the formation of immunosuppressive, fibrotic TME and poor CD8(+) cytotoxic T cell infiltration, the use of the selective FAK inhibitor VS-4718 reduced tumor fibrosis and decreased the amounts of tumor-infiltrating immunosuppressive cells that were accompanied by limited tumor progression and doubling of survival in a mouse model with human PDAC xenografts [52]. Here, PTK2 is linked to neoplasm.