Based on the observation that patients in our study had an overall controlled RA (showing low to moderate activity according to DAS-28 score and low inflammatory biomarkers) this model may also explain the significant increase observed in the IgG anti-ghrelin immune complexes percentage in the patients, besides the previously discussed affinity-mediated compensatory mechanism that may promote ghrelin immune complexes formation. The gene discussed is GHRL; the disease is rheumatoid arthritis.