Thus, although COLO205 and HT29 tumour cells have disabled multiple tumour suppressive mechanisms, including p53, and adapted to aberrant ERK1/2 activation arising from BRAFV600E mutation, sufficient ERK1/2-responsive tumour suppressive mechanisms remain intact to drive proliferative arrest or cell death following the hyperactivation of ERK1/2 that occurs upon MEKi withdrawal. This evidence concerns the gene TP53 and neoplasm.