To understand the molecular mechanism underlying the anti-MM effect by the dual blockade of RSK2-NTKD and AKT, the study performed gene expression profile (GEP) analysis to comprehensively analyze commonly modulated genes by the combinatory treatment with BI-D1870 and ipatasertib in comparison with those modulated either by BI-D8170 or ipatasertib alone in NCI-H929 and OPM-2 cells (Table S2). The gene discussed is AKT1; the disease is Miyoshi myopathy.