The ability to quantify inborn susceptibility using genome-wide polygenic scores is likely to be generalizable across a broad range of complex diseases, contingent upon availability of a large discovery GWAS, independent validation and testing datasets, and the heritability of a given disease explained by common variants (Torkamani et al., 2018). Predictive power will likely continue to improve in coming years as a function of larger discovery GWAS studies and improved computational algorithms that integrate functional genomics annotation, variant-variant interactions, and rare large-effect variants into the predictive model (Chatterjee et al., 2016; Zhang et al., 2018).
