In addition, in a model of PDAC, inactivation of the kinase activity of FAK in fibroblasts reduced fibrosis, immunosuppressive cell populations and tumour progression.102 However, by contrast, work from the Hodivala-Dilke group has shown that loss of FAK from CAFs can promote breast tumour growth through alterations in tumour metabolism.103 The use of different promoters to drive Cre recombinase-mediated fibroblast-specific deletion of FAK might represent targeting of distinct CAF subpopulations and explain the disparate results in these studies. Here, PTK2 is linked to breast neoplasm.