This result suggests that PI3Kα would be a target of choice for pancreatic cancer patients who, in spite of their genetic heterogeneity associated with class I PI3K activation (mutant KRAS, deletion of PTEN, mutation of PIK3CA), depend on intrinsic basal PI3Kα activity, thus corroborating the prognostic value of the PI3Kα activity signature to detect pro‐metastatic features (Fig 1). The gene discussed is KRAS; the disease is pancreatic neoplasm.