Assuming that the number of GWAS hits in each of these two diseases is correlated with the complexity of the genetic models (one for lactase persistence and 22 for melanoma), we can see that as the effect sizes decrease and the number of associating genes increases, which, presumably, is correlated with increasing complexity of the genetic architecture, ET was less effective in identifying previously known genes [29, 30]. This evidence concerns the gene LCT and melanoma.