Ten years ago, Nobel laureate Sydney Brenner remarked, “We don't have to search for a model organism anymore. Because we are the model organisms” (1). Indeed, over the past decade, we have deepened our understanding not only of how the genomic blueprint for human biology manifests physical and chemical characteristics (phenotype), but also of how traits can change in response to the environment. A better grasp of the dynamic relationship between genes and the environment may truly sharpen our ability to determine disease risk and response to therapy. A collection of human phenotypic data, and its integration with “omic” information (genomic, proteomic, transcriptomic, epigenomic, microbiomic, and metabolomic, among others), along with remote-sensing data, could provide extraordinary opportunities for discovery. A comprehensive “human phenomic science” approach could catalyze this effort through both large-scale “light” phenotyping studies and “deep” phenotyping studies performed in smaller groups of individuals.