Notably, different KRASMut tumour models respond very differently to MEKi treatment: acute myeloid leukaemia and colorectal cancer models evolved to amplify KRASMut, lost KRASWT and remained ERK1/2 dependent38; pancreatic ductal adenocarcinoma genetically engineered mouse models (GEMMs) subjected to MEKi + ERKi treatment amplified KRASG12D to maintain ERK1/2 signalling, whereas non-small-cell lung cancer GEMM models did not alter KRASG12D frequency and downregulated ERK1/2 signalling52. The gene discussed is MAPK3; the disease is neoplasm.