Nonetheless, considering the phenomenon where BAP1 mutations in specific tumor types lead to its sequestration within the cytoplasm and subsequent loss of enzymatic functionality, there remains a pressing need for additional investigative efforts to delineate therapeutic strategies that specifically target cytosolic BAP1.In fact, the NF-κB pathway is overactivated in a significant proportion of pancreatic cancer patients. This evidence concerns the gene NFKB1 and pancreatic neoplasm.