Importantly, clinical studies conducted in human peripheral blood mononuclear cells (PBMCs) demonstrated a downregulation of GANAB in interferon (IFN)β-treated humans compared to untreated controls, and an even greater GANAB downregulation in IFNβ treatment-responsive patients, thereby identifying this UPR mediator as a suitable biomarker for MS [46]. This evidence concerns the gene GANAB and myeloid sarcoma.