NK cell hypofunction is the most well documented immune abnormality in CFS patients (Brenu et al. 2016; Fletcher et al. 2010; Natelson et al. 2002) and there is evidence of abnormal metabolic pathways and impaired signalling activity known to be involved in endotoxin tolerance in this cell type extracted from CFS/ME patients both in terms of miRNA activity and impaired extracellular signal-regulated kinase 1/2, mitogen-activated protein kinase 1/2 and p38 signalling (Huth et al. 2016; Petty et al. 2016). This evidence concerns the gene MAP2K1 and myalgic encephalomeyelitis/chronic fatigue syndrome.