It is evident that under these conditions the normalisation of the melatonin level is not sufficient to correct metabolic disorder, which can be achieved by suppressing the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) or by inducing the nuclear-factor-E2-related factor-2 (Nrf2), antagonistic to NF-κB [9,10]. The gene discussed is NFKB1; the disease is metabolic disease.