Given my sceptical view that ORMDL3 is really an asthma gene (that may be even shared by the authors of the initial association) the train has now departed with more groups speculating about ORMDL3 function.
For example this new paper by Gerard Cantero-Recasens is about the unfolded protein response (UPR) that may be triggered by a putative loss of function mutation in ORMDL3 via a Ca2+ decrease in the ER. Although I am quite intrigued about the fact that the story now moves to calcium and vitamin D, we are far away from any conclusive evidence.
And here is another paper that associates ORMDL3 to the sphingolipid metabolism. Although that may be also an interesting pathway (given a bulk of literature not cited in the paper ( more, more, more, more) I still wonder if this is wishful thinking. The authors do not touch the main problem – the weak connection of some genomic variants in that region to ORMDL3 function to asthma pathogenesis.