So are you saying that even though Ariad's 113 could be more potent against ALK, the cancer develops resistance through other pathways that '113 doesn't inhibit?
many—perhaps even most—cases of resistance to Crizotinib stem from reasons other than a mutation in ALK.
That might stem from the fact that Crizotinib isn't a great ALK-inhibitor in the first place (it was not in fact specifically developed as one - it's actually a dual cMET/ALK drug). Resistance develops when you only partially knock down a pathway - that way you have cells mutating under selective pressure - whether by furhter ALK mutations or via new pathways. If you can knock down the pathway better from the outset, there is less chance of resistance developing.
Preclinically, '113 is a way better drug than Crizotinib - more potent by a factor of 10, much more selective against wild-type ALK and having a factor of 10 better therapeutic index.
Market Data 
Markets 
AI
