These observations are supported by several reports on the crosstalk between UPR and mTORC1 pathway in the cells contributing to malignancy cells14,16–18 and provide the mechanistic rationale to mTOR inhibitors as a useful regimen to potentially improve treatment efficacy for MM and RRMM in combination with proteasome inhibitors24,26–28. This evidence concerns the gene MTOR and Miyoshi myopathy.