However, it was a perplexity to explain why the breed with thickest backfat could house so many coexisting anti-obesity marker bacteria in SHBS and BHBS; rather, it might be the breed advantage of SHBS and BHBS, or it might be the fat deposition genes of the hosts, such as IRX3, THY1, PLIN4, LPL, CFD, SREBP1, C/EBPα, C/EBPβ, C/EBPδ, and ATGL [25,26] exerting a stronger effect on fat metabolism instead of intestinal microbiota. Here, LPL is linked to obesity due to melanocortin 4 receptor deficiency.