Interestingly, a recent study found that activated PI3K signalling could phenocopy mutant Kras in a mouse model of pancreatic cancer, and concluded that KRAS acts through PI3K signalling to induce cancer.35 While the authors suggested that therapeutic targeting of PI3K signalling might be a promising approach for the treatment of pancreatic cancer, our data indicate that response to treatment will be dependent on the combination of genetic events in individual tumours. The gene discussed is KRAS; the disease is neoplasm.