Recent studies suggest that MM at relapse has a more complex genetic landscape compared to primary tumors and highlights the biological role of TP53 inactivation and certain structural genome rearrangements (e.g., 1q gain, del(17p), and MYC translocations, see Section 5.1) rather than mutations in genes associated with resistance to PIs or IMiDs in acquired resistance to therapy [25,54,60]. The gene discussed is TP53; the disease is Miyoshi myopathy.