These results clearly demonstrate that ERK1/2 signalling normally limits the extent of ER stress-induced death in a variety of cell types and adds to growing evidence that this aspect of ERK1/2 survival signalling is co-opted by tumour cells; for example, MEK1/2 inhibition sensitises melanoma cells to ER stress-induced cell death [51]. This evidence concerns the gene MAPK3 and neoplasm.