As an example, targeting FAK genetically in FSP‐positive CAFs resulted in metabolic switching of the malignant tumour, more aggressive growth, enhanced inflammatory chemokine signalling, and a switch in tumour metabolism [58]; FAK is a key regulator of myofibroblast function and this study concurs with other interventions suppressing myCAF function in PDAC tumours [25, 26, 29, 30]. This evidence concerns the gene PTK2 and neoplasm.