Furthermore, the functional insights of the immune response in IMN patients have enabled us to highlight a possible involvement of ficolin-2 (FCN2) as a novel potential actor in IMN pathogenesis, since (i) it already demonstrated its capability to turn on the lectin-mediated complement pathway, whose activation was shown to be sustained in IMN affected podocytes by the interaction between anti-PLA2R IgG4 and mannose-binding lectin (MBL), and (ii) that IMN can also develop in subjects with MBL deficiency. The gene discussed is FCN2; the disease is hyperinsulinemic hypoglycemia, familial, 4.