It was demonstrated that monogenic obesity genes are over-represented near identified loci, and several complex association signals near LEPR and KLF14 point towards a major contribution for common variation affecting the leptin–melanocortin system in early life [52]; GHSR resulted in a viable receptor for the treatment of obesity [53]; CNR1 was linked to diabetic nephropathy [54]; a noticeable reduction in lipid accumulation was also found in extract-treated cells through the H1R1 genes in 3T3-L1-differentiated mouse cells. Here, LEPR is linked to obesity due to melanocortin 4 receptor deficiency.