It would also be informative to combine the loss of DUSP5 and DUSP6 with alterations in other tumour suppressor genes known to be involved in pancreatic carcinogenesis such as p53, CDKN2A (encoding p16) or SMAD4. The fact that DUSP5 and DUSP6 have at least partially non-redundant functions despite regulation of a common target (ERK) in this disease model may reflect the differential regulation of ERK in either the cell nucleus or cytoplasm. Here, SMAD4 is linked to neoplasm.