Since specific genetic driver lesions had been repeatedly found to be associated with human MM by the year 2008, particularly alterations of the CDKN2A, NF2, and TP53, Jongsma et al. decided to establish whether various genetic alterations affecting the same signaling pathways that are dysregulated in the human disease counterpart might similarly induce MM in rodents in the absence of carcinogenic exposure to asbestos (64). The gene discussed is TP53; the disease is Miyoshi myopathy.