Of note were FAK over-expression and activation, as a crucial feature in the majority of human PDAC epithelia, to be a principal driver in PDAC desmoplasia and the generation of an immunosuppressive TME [21], since intratumoral regulatory T cells (Treg) were up-regulated by FAK-dependent expression of CC-chemokine ligand 5 (CCL5) and the cytokine transforming growth factor β2 (TGF-β2) [24], the FAK inhibitor defactinib (also known as VS-6063) has been shown to inhibit FAK overexpression and effectively reduce the formation of tumor stroma in PDAC [25]. This evidence concerns the gene PTK2 and neoplasm.