suggested that targeting MALAT1 by an LNA‐gapmeR antisense oligonucleotide (ASO) suppresses MM cell proliferation and induces apoptosis in a murine xenograft model of human MM.[47] Intriguingly, a recent study demonstrated that MALAT1 ASO delays primary tumor growth and improves the responses to chemotherapy or ICB therapy in triple‐negative breast cancer (TNBC) mouse models.[48]MALAT1 inhibition decreases the immunosuppressive function of myeloid cells, including TAMs, and increases T‐cell infiltration in the TME. Here, MALAT1 is linked to Miyoshi myopathy.