The genetic CAF depletion in transgenic mice using fibroblast activating protein (FAP) promoter-driven diphtheria toxin receptor [97] or αSMA-thymidine kinase [27] led to contradictory results as in the first case pancreatic ductal adenocarcinoma growth was slowed down [97] while, in the second case, it became more aggressive and invasive, leading to shorter animal survival [27]. The gene discussed is ACTA1; the disease is pancreatic ductal adenocarcinoma.