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Auranofin treatment alone was sufficient to induce a modest level of ER stress, seen in upregulation of UPR target genes in the absence of any other ER stress stimulus (Figure 3E)

Nevertheless, future research should focus on examining temporal relationships between HPA axis function and immune-inflammatory or nitrosative stress pathways through biomarkers like TNF-, IL-10, TGF-, inducible NO synthase, NO production, protein nitrosylation, and bacterial translocation in ME/CFS patients to better understand their roles [79]

Its targeted fragment design makes it useful in research focused on body composition signaling without the full hormonal profile of upstream GH stimulators