A recent study demonstrated that blocking the oncogenic KRAS gene led to an increase in the expression of HER2 and HER3 in both human and mouse pancreatic cancer models, which led cancer cells to rely on NRG1 secreted by CAFs as a critical factor for survival [98] such a mechanism involving CAFs might also functional during KRASG12C inhibition in our model, which determines treatment response. The gene discussed is KRAS; the disease is familial pancreatic carcinoma.