We had earlier used array based comparative genomic hybridization and gene expression microarrays to identify a recurrent deletion in pancreatic cancer harbouring the ARID1B gene; that encodes one of the four alternative DNA-binding components of the human SWI/SNF chromatin remodeling complex. We have now shown that inactivation of the nuclear localisation signal of ARID1B causes its cytoplasmic sequestration where it exhibits a gain of oncogenic function by activating ERK and Wnt signalling. In a parallel study, we have identified a potential role of ARID1B in nuclear processes including mitosis, enhancer mediated gene activation and alternative splicing. Current efforts are focused to unravel mechanistic basis for these non-canonical roles of ARID1B.