Null mutations in the human FTO gene, an AlkB subfamily member that reverses m6A methylation through oxidation, link to an autosomal-recessive lethal syndrome in humans [106], and individuals with intron mutations in FTO displayed increased risk of obesity and type 2 diabetes [107,108], indicating that m6A RNA methylation plays a role in the aetiology of metabolic diseases. This evidence concerns the gene FTO and obesity due to melanocortin 4 receptor deficiency.