Applied to novel genes such as the ones identified in this study with no previous link to adipocyte function (DNLZ, VARS2, COL4A3BP, USP37, and TSPAN15), transgene complementation with human coding variants reading out “rescue” of the identified morphologic profile with correlation to metabolic disease phenotypes would provide strong evidence for disease causation and direction of effect. This evidence concerns the gene DNLZ and metabolic disease.