Thus, in KRASMut tumours the response to ERK1/2 pathway inhibition is complicated by the diversity of RAS effector pathways and codon-dependent differences in effector pathway use, whereas tissue-specific differences in mutant allele frequency will further complicate how tumours evolve to ERK1/2 pathway inhibition, including whether they remain ERK1/2 dependent. This evidence concerns the gene MAPK3 and neoplasm.