In addition, during obesity B cell activating factor (BAFF) levels have been found elevated in both mice and humans [88–90], where it not only promotes breaking of the peripheral tolerance by suppressing Tregs, but also facilitates the metabolic reprogramming of B cells through increasing both glycolysis and OXPHOS, enhancing antibody production upon LPS stimulation [91], while allowing autoreactive B cells to evade deletion at post-GC checkpoints [92]. The gene discussed is TNFSF13B; the disease is obesity due to melanocortin 4 receptor deficiency.