This dominant effect may be explained by the central role of CatS in periodontal-specific mechanisms such as biofilm-induced immune activation, lysosomal protease activity, antigen presentation via MHC class II, and Th17-mediated inflammation, rather than in obesity-related pathways like systemic low-grade inflammation or adipokine imbalance [26, 27]. The gene discussed is PIMREG; the disease is obesity due to melanocortin 4 receptor deficiency.