Comprehensive genomic studies have revealed frequent deletions or loss-of-function mutations of tumor suppressor genes (TSGs) in MPM, most often cyclin-dependent kinase inhibitor 2A (CDKN2A), BRCA1 associated protein-1 (BAP1) and neurofibromatosis type 2 (NF2) (4, 5) (Figure 1A), for which direct targeting has proven difficult, contrasted to oncogene-driven malignancies that benefit from a vast majority of molecular targeted anti-cancer drugs. Here, BAP1 is linked to cancer.