MPM exhibits a distinct genomic signature, including inactivating mutations in cyclin-dependent kinase inhibitor 2A (CDKN2A), and more recently, ubiquitin carboxyl-terminal hydrolase (BAP1) and neurofibromin 2 (NF2), have been shown to be the most prevalent in this type of cancer (Figure 1A). The gene discussed is BAP1; the disease is cancer.