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CA IX directly participates in these hallmarks, as supported by the fact that its suppression, mutation/deletion, pharmacologic inhibition, or treatment with monoclonal antibodies result in significantly reduced growth of tumor xenografts in vivo [48, 61,62,63,64]

Increasing evidence demonstrates acetylcholine receptor and transient receptor potential ion channel dysfunction in ME/CFS, though how these findings could translate to a diagnostic biomarker are yet to be explored