Additionally, combination therapies with PARP1 inhibitors or bortezomib synergistically reduce MM viability [167,168] (see Supplementary Tables S1 and S2, which comprehensively summarize MALAT1’s oncogenic functions, biomarker correlations, preclinical targeting evidence—including the clinical-stage ASO FTX-001—and patient-derived data directly supporting its central role in proliferation, chemoresistance, hypoxia adaptation, and microenvironment remodeling in MM). The gene discussed is PARP1; the disease is Miyoshi myopathy.