For example, whereas inhibition of FAK in a mouse model for pancreatic cancer attenuated the cancer-promoting activity of the fibrotic stroma, limited tumour progression and enhanced survival,138 depletion of CAFs, which might be expected to have a similar effect, actually led to more aggressive tumours and reduced survival.139 One explanation is the heterogeneity of CAFs in pancreatic and other cancers that may have diverse impacts on tumour growth and progression within the TME, including immune-modulation.140,141. This evidence concerns the gene PTK2 and neoplasm.