The IDO2 genetic observation is not necessarily tied to the IDO metabolic trap hypothesis, although it does agree with it. The data tells us that a faulty IDO2 is very likely required to develop ME/CFS, along with perhaps some other genes like
@Cam Newton mentioned. But that only brings us one step closer to the IDO1 trap theory. It could also be that IDO2 serves some other role that keeps people with a functioning IDO2 from developing ME/CFS, it may not necessarily tie to the trap model of Robert Phair.
One thing that concerns me a bit is how common this IDO2 mutation is. Robert Phair was originally looking for mutations that were not rare (by rare is probably implied something like less than 1% of population), but now we have found a mutation that affects the majority of the population. If 0.5% of the entire population gets ME/CFS, then with 75% having a faulty IDO2, if you belong to the faulty IDO2 group, you still only have a 0.66% likelihood of getting ME/CFS. In other words, a lot that has to go wrong for someone to develop ME/CFS even with a faulty IDO2.
To contrast it with some other disease causing mutations, for example there is a well known BRCA mutation that is tied to breast cancer. It is estimated that a massive 70% of women with BRCA mutation develop breast cancer during their lifetime, as opposed to around 12% in the general population.