The researchers have identified molecular pathways that could contribute to the pathogenesis of the phenotype and that are represented by: (i) type 1 (T1) immune response driven by interferons (IFN), (ii) type 3 (T3) inflammation mediated by Th17 cytokines, (iii) systemic inflammation associated with IL-6 release and obesity, and (iiii) lack of inflammatory processes resulting in paucigranulocytic phenotype. The gene discussed is IL6; the disease is obesity due to melanocortin 4 receptor deficiency.