To assess the performance and to determine the limits of our approach, we applied ET to a number of phenotypes that vary in presumed genetic architecture, ranging from an essentially Mendelian trait (lactase persistence), to diseases of increasing complexity, i.e., melanoma, representing an oligogenic disease, and fasting glucose/Type 2 diabetes mellitus as a highly complex disease with many genes of small effect. Here, LCT is linked to diabetes mellitus.