In summary, we demonstrated that H19 inhibited apoptosis of MM cells and promoted BTZ resistance by regulating the translation of MCL-1 and targetedly silencing miR-29b-3p, suggesting that H19/miR-29b-3p/MCL-1 may be a novel and promising therapeutic target for coping with drug resistance in MM treatment. Here, H19 is linked to Miyoshi myopathy.