In spite of this, considering the capacity of BAP1 to poly-deubiquitinate several protein targets, and that BAP1 has been shown to prevent these targets from proteasomal degradation, it was hypothesized that the BAP1 tumor suppressor trait could reside at least in part in the regulation of protein stability in the nucleus through its deubiquitinase function. Here, BAP1 is linked to neoplasm.