The repressing effects of YTHDF1 knockdown on levels of glycolysis-enhancing genes, glucose uptake, lactate production, cell viability, and proliferation percentage in MM cells were partially nullified by overexpression of FOXM1 (P < 0.05, Fig. 7B-F), as well as the promotional effects on the aggregation of G0/G1 phase cells and apoptosis (P < 0.05, Fig. 7G/H). The gene discussed is FOXM1; the disease is Miyoshi myopathy.