Our hypotheses were focused on the following problems: (a) failure to observe a significant EBF1 gene-by-stress association in Black samples, (b) observing a significant association only in a specific subgroup of samples (i.e., White females), and (c) extending our understanding of the clinical implications of race and sex-specific gene-by-stress associations linking to a path from EBF1 and stress to obesity to fasting blood glucose to the development of cardiometabolic disease risk (e.g., type 2 diabetes mellitus). This evidence concerns the gene EBF1 and obesity due to melanocortin 4 receptor deficiency.