The proopiomelanocortin gene (POMC) is expressed in the hypothalamus, in the pituitary gland. It yields a range of biologically active peptides and hormones and undergoes tissue-specific posttranslational processing to yield a range of biologically active peptides producing adrenocorticotropic hormone (ACTH), b-endorphin, and a-, b- and c-melanocyte-stimulating hormone (MSH). These peptides then interact with different melanocortin receptors (MCRs) and are involved in a wide range of processes including the regulation of body weight (MC3R and MC4R), adrenal steroidogenesis (MC2R) and hair pigmentation (MC1R). Published in the British Associations of Dermatologists in 2012, Lack of red hair phenotype in a North-African obese child homozygous for a novel POMC null mutation showed nonsense-mediated decay RNA evaluation in a hair pigment chemical analysis. They found that inactivating the POMC gene mutation results in obesity, adrenal insufficiency, and red hair. This has been seen in both in humans and mice. In this experiment they described a 3-year-old boy from Rome, Italy. He was a source of focus because he had Addison's disease and early onset obesity. They collected his DNA and amplified it using PCR. Sequencing analysis revealed a homozygous single substitution determining a stop codon. This caused an aberrant protein and the corresponding amino acid sequence indicated the exact position of the homozygous nucleotide. The substitution was localized in exon 3 and nonsense mutation at codon 68. The results from this experiment strongly suggest that the absence of red hair in non-European patients with early onset obesity and hormone deficiency does not exclude the occurrence of POMC mutations. By sequencing the patients DNA they found that this novel mutation has a collection of symptoms because of a malfunctioning nonsense-mediated mRNA decay surveillance pathway.