A central goal of human genetics is to understand the links between genetic variation and disease. Intuitively, one might expect disease-causing variants to cluster into key pathways that drive disease etiology. But for complex traits, association signals tend to be spread across most of the genome, and most heritability is driven by variants near genes without any obvious connection to disease. In a 2017 paper we argued that there is a need for new conceptual models for the molecular processes that link variation to complex phenotypes. We proposed a model in which gene regulatory networks are sufficiently interconnected that all genes expressed in disease-relevant cells are liable to affect the functions of core disease-related genes and that most heritability is driven by effects on genes outside core pathways. We refer to this hypothesis as an "omnigenic" model. In this talk I will review our 2017 paper and describe our more recent work on this problem. I will close with my thoughts on future directions in the field.