Furthermore, since the pathogenesis of MM can be dependent on increased MYC protein expression and there was an increase in MCT1 mRNA expression in MM CD138 + cells compared to MGUS CD138 + cells, an assessment of the correlation of MYC with MCT1 and MCT4 expression was performed using MYCi975, which is a MYC inhibitor that engages MYC intracellularly and disrupts MYC/MAX-dimers that impairs MYC-driven gene expression. Here, SLC16A1 is linked to Miyoshi myopathy.