Thagard draws attention to both statistical evidence that suggests ulcers are somehow associated with H. pylori, as well as mechanistic evidence that can explain how the agent of infection could persist in a hostile environment long enough to cause an ulcer. More recently, philosophers interested in evidence-based medicine have probed the relationship between these two types of evidence in the health sciences. Russo and Williamson argue that both types of evidence are necessary to justify causal inference; the correlational evidence establishes that there is a difference-making relation between some cause and some effect, while the mechanistic evidence establishes how exactly the cause produces its effect—the “Russo-Williamson Thesis” (Russo and Williamson 2007). Philosophers have since refined the Russo-Williamson Thesis, pointing out, for instance, that “type of evidence” could refer to different methodologies for gathering evidence or to different objects of evidence.  Difference-making methodologies include observational studies and randomized controlled trials, while mechanistic methodologies include interventionist experiments such as those described above; likewise, the object of evidence could be the evidence of an associated difference or it could be the evidence concerning the mechanism linking the cause and effect (Illari 2011; see also Campaner 2011).  Evidence-based medicine hierarchies, which rank different kinds of evidence in terms of its epistemic strength, tend to prioritize evidence from difference-making methodologies (such as randomized controlled trials and meta-analyses) over mechanistic evidence; in reply, these philosophers argue that the different types of evidence are on a par (each with its own strengths and weaknesses) and advocate for integrating difference-making and mechanistic evidence, a sentiment which aligns with the emphasis on mechanism integration discussed in Section 5.2 above (Clarke et al. 2013, 2014). 