Mechanistically, the dysfunction of adipogenic differentiation might be associated with impaired modulation between SCARA3 and JUN. Further studies will be worthy of being performed to validate the role of SCARA3, such as the phenotypical observation of Scara3 knock-out mice and the methylation of SCARA3 promoter in mice with obesity. This evidence concerns the gene JUN and obesity due to melanocortin 4 receptor deficiency.