Bacterial LPS-induced inflammation may induce TNFRSF12A expression via TNFα signaling [75]; thus, the observed Tnfrsf12 overexpression may be induced by an extracellular stimulus, e.g., LPS derived from obesity-related gut bacterial species [76]. This evidence concerns the gene TNFRSF12A and obesity due to melanocortin 4 receptor deficiency.