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As Ca 2+ is required for many NK cell functions, including cytotoxic activity, formation of the immune synapse, the granule-dependent pathway of apoptosis, microtubule reorganisation and cytokine gene transcription [62, 196], impaired TRPM3-dependent Ca 2+ signalling may contribute to the NK cell dysfunction seen in ME/CFS
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Additionally, one study indicated that HMGB1 can upregulate heme oxygenase 2 and transferrin expression through the RAS-JNK/p38 pathway, promoting erastin-induced ferroptosis [101]