Finally, targeting PRKCN with an orally bioavailable inhibitor suppresses MM cell growth and overcomes drug resistance in vitro, and elicits robust efficacy in cell line-derived xenografts and a patient-derived xenograft, which is connected with the mitigated PRKCN expression and activation loop phosphorylation as well as blunted mTOR-IRF4 axis. This evidence concerns the gene IRF4 and Miyoshi myopathy.