Along these lines, focal adhesion kinase (FAK) activation downstream of integrin binding to fibronectin and collagens correlates with high levels of fibrosis and poor CD+ cytotoxic T cell infiltration in PC; FAK inhibition limited tumor progression, markedly reduced tumor fibrosis, decreased the numbers of tumor-infiltrating immunosuppressive cells, and rendered the previously unresponsive KPC mouse model responsive to T cell immunotherapy and programmed cell death protein (PD)-1 antagonists. The gene discussed is CTLA4; the disease is neoplasm.