Inflamm-aging results from the activation of signaling networks critical to inflammation, such as those regulated by the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) transcription factor, particularly when combined with a variety of stimuli, such as senescent cells, obesity, circulating mitochondrial DNA, gut microbiota and diet triggering and sustaining inflammatory conditions (58, 63–68). This evidence concerns the gene NFKB1 and obesity due to melanocortin 4 receptor deficiency.