Some studies have examined the effect of ablating the prominent CAF subtypes on carcinogenesis: deletion of FAP-expressing fibroblasts induced rapid tumour necrosis in LLC14 and impeded metastasis in PDAC,68 whereas elimination of α-SMA fibroblasts enhanced tumorigenesis in both mouse and clinical models.8,59 CAF-directed therapy should therefore be designed against specific pro-tumour factors or functions with the aim of preventing CAF function or activation, or reprogramming CAFs back into a normal, resting phenotype. The gene discussed is ACTA1; the disease is neoplasm.