Mechanistically, this result was attributed to the secretion from FAK-deficient CAFs of exosomes enriched with the tumour-suppressive microRNAs miR-16 and miR-148a, which suppressed an EMT and migratory phenotype in the cancer cells.101 These data unveiled an additional role for FAK signalling in the tumour stromal compartment, promoting a more migratory and metastasis-competent phenotype. Here, PTK2 is linked to neoplasm.