These results raise the question as to why the variants detected in this large study only explain a small fraction of the inherited variability in BMI. There are several possible explanations, which require further experimentation to explore. First, there may be many more loci with common variants that influence BMI. We can predict that additional loci will be discovered by similarly sized studies in new samples: because we had only 5–10% power to detect variants such as those at KCTD15, MTCH2 and NEGR1, dozens of additional variants with comparable effect sizes likely remain unidentified. The number of common variants with smaller effects, and which might be detected with larger samples, is harder to predict, as this depends on the allelic architecture; if the number of causal variants increases as effect sizes decrease, then increasing sample size will be especially productive. Modifying effects such as interactions with environmental factors, other genetic variants, age, sex or other variables may, if substantial, also diminish apparent effect sizes, so detailed analyses of interaction with validated variants may be informative. Finally, other than the MC4R
