Glucocorticoid resistance does not explain most of the evidence gathered so far. In fact major reviews and models have been written trying to explain findings of enhanced GCr sensitivity, which makes the most sense given all of the neuroendocrine studies so far in CFS.
The best (in my opinion) review of the neuroendocrine findings, despite being out of date and written by a protege of an unpopular psychiatrist is still this one:
http://www.ncbi.nlm.nih.gov/pubmed/1270018 (Cleare 2003)
There was a more recent attempt, but I was not as impressed:
http://www.hindawi.com/journals/isrn/2013/784520/ (Tomas, Julia Newton, Watson 2013)
(Anyone who is seriously interested in this stuff needs to read the above two articles).
The SNPs found by the CDC group, in the papers mentioned by
@Helen have been suggest as a possible cause for this increased sensitivity (note again: opposite of resistance). And indeed this assumption is specifically mentioned in these papers (which does have some author continuity)
http://www.ploscompbiol.org/article/info:doi/10.1371/journal.pcbi.1000273
http://www.plosone.org/article/info:doi/10.1371/journal.pone.0084839
Glucocorticoid resistance might be a problem in a few people, but it does not fit with the rest of the evidence gathered in CFS so far.
If there is a central problem here, then I am willing to bet that it will be something other than GCr SNPs, or alpha/beta ratios.