The findings of a preclinical study, involving both genetically engineered and patient-derived mouse models of pancreatic cancer, indicate that the Rho kinase (ROCK) inhibitor fasudil is able to disrupt the extracellular matrix (ECM) of tumours, and thus improve exposure to subsequent treatment with chemotherapy. Crucially, a graded response to fasudil priming was observed, whereby the presence of high levels of fibrillar collagen in pretreatment tumour biopsy samples was able to predict a positive response to fasudil priming. In addition to effects on the ECM, fasudil was also shown to confer an increase in tumour blood flow, and hence drug delivery, owing to the clinically recognized vasodilatory effects of this agent. These promising preliminary results indicate a need for further investigations of this approach.