Combined MEK1/2 and BCL2/BCL‐XL inhibition is also effective in KRAS‐mutant lung and pancreatic tumour cells 86, 87 and acts ‘on target’ since cell death was caspase‐dependent, required BAX and BAK 60 and was confined to tumour cells addicted to ERK1/2 signalling 60, 84, 86, 88. The gene discussed is BAX; the disease is neoplasm.