A substantial argument in favor of the pathophysiological significance of SRA1 as a regulatory molecular signal in obesity lies in its variable expression that we observed between non-diabetic NW and obese people, implying that further clinical studies, preferably longitudinal, and including larger cohorts as well as experimental studies of loss and gain of function approaches will be needed to understand the SRA1-associated underlying molecular mechanisms at the genetic and epigenetic levels that regulate metabolic disease pathogenesis. This evidence concerns the gene SRA1 and metabolic disease.