The robust generation of M2 macrophages, particularly the CD163+ subpopulation, and CAFs by asbestos contributes to an immunosuppressive TIME in Bap1-mutant mice, suggesting that chemoprevention or immunotherapeutic strategies targeting CD163+ TAMs, CD39/CD73-adenosine, and Ccl2/Ccr2−IL6/IL10 signaling might reprogram MM from a tumor-promoting “M2-like” phenotype to a tumoricidal “M1-like” phenotype, potentially benefitting BAP1 mutation carriers and others with germline pathogenic mutations. The gene discussed is BAP1; the disease is Miyoshi myopathy.