The idea that MKPs can intervene to prevent the engagement of tumour suppressive pathways has been suggested previously, mainly in the context of ERK-dependent oncogene-induced senescence (OIS) [166] and, as discussed previously, there is some support for differential outcomes in terms of cell proliferation and senescence after deletion of the inducible nuclear ERK-specific MKP DUSP5 in cells expressing either activated Ras or Braf [131]. Here, MAPK1 is linked to neoplasm.