It's questionable whether the smoking lesion problem is a valid counterexample to EDT in the first place. It can be argued that the problem is underspecified, and it requires additional assumptions for EDT to determine an outcome:
A reasonable assumption is that the rare gene affects smoking only though its action on Susan's preferences: "Susan has the generic lesion" and "Susan smokes" are conditionally independent events given "Susan likes to smoke". Since the agent is assumed to know their own preferences, the decision to smoke given that Susan likes to smoke doesn't increase the probability that she has the genetic lesion, hence EDT correctly chooses "smoke".
But consider a different set of assumptions: an evil Omega examines Susan's embryo even before she is born, it determines whether she will smoke and if she will, it puts in her DNA an otherwise rare genetic lesion that will likely give her cancer but causes no other detectable effect.
Please note that this is not a variation of the smoking lesion problem, it's merely a specification which is still perfectly consistent with the original formulation: the genetic lesion is positively correlated both with smoking and cancer.
What decision does EDT choose in this case? It chooses "Don't smoke", and arguably correctly so, since that with these assumptions the problem is essentially a rephrasing of Newcom's problem where "Smoke" = "Two-box" and "Don't smoke" = "One-box".
I agree with this analysis. The most interesting case is a third variation, in which there is no evil Omega, but the organic genetic lesion causes not only a preference for smoking but also weakness in resisting that preference, propensity for rationalizing yourself into smoking, etc. We can assume happens in such a way that "Susan actively chooses to smoke" is still new positive evidence to a third-party observer that Susan has the lesion, over and above the previous evidence provided by knowledge about Susan's preferences (and conscious reasoni...
I stumbled upon this paper by Andy Egan and thought that its main result should be shared. We have the Newcomb problem as counterexample to CDT, but that can be dismissed as being speculative or science-fictiony. In this paper, Andy Egan constructs a smoking lesion counterexample to CDT, and makes the fascinating claim that one can construct counterexamples to CDT by starting from any counterexample to EDT and modifying it systematically.
The "smoking lesion" counterexample to EDT goes like this:
EDT implies that she should not smoke (since the likely outcome in a world where she doesn't smoke is better than the likely outcome in a world where she does). CDT correctly allows her to smoke: she shouldn't care about the information revealed by her preferences.
But we can modify this problem to become a counterexample to CDT, as follows:
Here EDT correctly tells her not to smoke. CDT refuses to use her possible decision as evidence that she has the gene and tells her to smoke. But this makes her very likely to get cancer, as she is very likely to have the gene given that she smokes.
The idea behind this new example is that EDT runs into paradoxes whenever there is a common cause (G) of both some action (S) and some undesirable consequence (C). We then take that problem and modify it so that there is a common cause G of both some action (S) and of a causal relationship between that action and the undesirable consequence (S→C). This is then often a paradox of CDT.
It isn't perfect match - for instance if the gene G were common, then CDT would say not to smoke in the modified smoker's lesion. But it still seems that most EDT paradoxes can be adapted to become paradoxes of CDT.