Because OMIM is a manually curated database, it is possible that known drug mechanisms influence OMIM entries, creating a positive association between OMIM genetic evidence and approval. However, we observe a positive effect of OMIM genetic associations reported by Nelson et al. 2015 on progression events occurring after data were collected for that paper, which is inconsistent with this reverse causal hypothesis. It is also possible these progression events are not truly independent of pre-2013 approvals, because they may represent approval for an indication similar to the original indication. However, the positive effect of OMIM genetic evidence on 2013-18 progression remains significant when targets with pre-2013 approvals for similar indications are excluded (S11 and S12 Tables). Another possibility is that the success of OMIM is due to treatments such as protein replacement therapies for monogenic diseases, which may have higher success rates as a whole [25]. However, we still find a large positive effect of OMIM genetic evidence when we exclude hereditary diseases and MeSH terms mapped to OMIM phenotypes from the analysis (S21 Table, S27 Fig). We conclude the
