I don't think that's quite right? There's been a fair amount of evidence pointing at possible issues, but there's no clear answer due to poor (or just different) study design, small sample sizes, different criteria across studies, different sample groups, etc.

So eg https://translational-medicine.biomedcentral.com/articles/10... reviewed 19 studies, many of which did find "evidence of mitochondria problems", but concluded:

> ...it is difficult to establish the role of mitochondria in the pathomechanisms of ME/CFS/SEID due to inconsistencies across the studies. Future well-designed studies using the same ME/CFS/SEID diagnostic criteria and analysis methods are required to determine possible mitochondrial involvement in the pathomechanisms of ME/CFS/SEID. [...] There is consistent genomic research suggesting that ME/CFS/SEID is not a primary mitochondrial disorder, however, mitochondrial decline might occur due to secondary effects of other disrupted pathways. [...] As population samples were small, these results should be interpreted cautiously.

I wouldn't summarise that as "no evidence". It's more like "ME/CFS doesn't seem to be a genetic disorder causing defective mitochondria, and the mitochondria look the same, but they seem to function differently for some reason even if we lack enough data to figure out why yet". Note that, eg, of the 19 studies reviews, 5 tried to check for differences in mitochondrial respiration between ME/CFS patients and healthy controls, and 4 of the 5 found notable differences; one study was able to reliably detect if a cell sample came from a ME/CFS patient or a healthy control based on measuring mitochondrial respiration.

I don't know that's enough to fully reject the null hypothesis just yet, but it's certainly not clear we can accept it either.