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In the past two decades, investigators have turned their attention to the development of new approaches to inhibit the aggressive behaviour of the tumour microenvironment (TME) of pancreatic ductal adenocarcinoma (PDAC),1–7 a dismal disease predicted to be the second leading cause of cancer death by 2030. However, complete genetic or pharmacological ablation of stroma results in more aggressive tumours. Furthermore, targeting the TME in patients with PDAC has grown controversial due to failure of clinical trials to improve patient survival.8 9 Together, these findings highlight the need to increase our understanding of the role of TME components (cellular and non-cellular) and their interplay in PDAC pathogenesis. This would better inform development of new treatment approaches not aimed at total stromal depletion, but rather TME reprogramming to ‘activate’ its antitumoural functions or to facilitate sensitivity to specific targeted therapies. In Gut, Jiang and colleagues elegantly report a novel therapeutic approach through partial stromal depletion, employing clinically available focal adhesion kinase (FAK) inhibitors to sensitise PDAC to signal …