one hundred of them. This contrasts with the conclusion reached by Purcell et al. (2009) in their models that simulated both disease status and genotype data, asserting that rare variants could not alone account for R2 signals generated from genome-wide, polymarker scoring of psychiatric disorders such as schizophrenia. This discrepancy between the studies may stem from design differences, as our simulations are based on real genotype data, which could have produced divergent features in the respective LD structures, or perhaps be a reflection of fundamental differences in the genetic architectures of these two psychiatric disorders.
