Furthermore, although most human MMs exhibit somatic alterations of BAP1, NF2, and/or CDKN2A—with 25/74 cases of MPM in the TCGA series having alterations of all three TSGs in combination (13)—it was not known if loss of BAP1 could cooperate with the inactivation of NF2 and/or CDKN2A to initiate a more aggressive form of MM. Here, CDKN2A is linked to Miyoshi myopathy.