That is an interesting point. It is true that CYP 2E1 is involved in the metabolism of both kava and acetaminophen (as well as another CYP enzyme) so you might think the effect would cancel out like that, but in both cases the situation is complex: there are other mechanisms/second pass metabolism that could also potentially interact. (for instance, NAPQI itself is metabolized by glutathione, which it has been suggested kava can deplete...) So just knowing that, I think the only thing you could predict is that there
could be an interaction, not whether the interaction would be "bad" or "good". And we actually know more than that because of this experiment where they found that kava aggravates the toxic effect of acetinophen in rat livers, meaning the same thing could possibly happen in human livers:
Yang, Xi, and William F. Salminen. "Kava extract, an herbal alternative for anxiety relief, potentiates acetaminophen-induced cytotoxicity in rat hepatic cells." Phytomedicine 18.7 (2011): 592-600.
So based on that I would still really recommend against the combination.