Furthermore, in a context of early pancreatic cancer lesions induced by oncogenic KRAS in an inflammatory condition (caerulein injections), the highly selective pharmacological inactivation of PI3Kα with another compound, namely GDC‐0326, completely prevented the maintenance of pre‐cancer lesions (Appendix Fig S16A–D), and features linked to stromal remodelling (Appendix Fig S16B and E). The gene discussed is KRAS; the disease is familial pancreatic carcinoma.