Although EGFR TKI's seem to antagonize chemo when it is combined with chemo - they do have single agent activities for tumors with EGFR mutation, and at worst a non-activitiy for those without EGFR mutation. The gist of IPASS study which you cited was that among patients without EGFR mutation, EGFR TKI doesn't do as well a job as platinum-containing doublet.
You are right that was making a hidden (and therefore questionable) assumption - that traditional chemo works fairly uniformly across kinome profiles in treatment naive patients. Thus the study is not despositive for acceleration. My bad. Thanks for the correction.
With that in mind, BATTLE trial provided a hint that single agent Sorafenib works in a Kras mutant subset of the EGFR Mutation negative subset which is known to be resistant to EGFR TKI