Given the fact that a substantial proportion of the world’s population have their bodyweight subtly influenced by SNPs in FTO, can FTO ever be considered a realistic pharmaceutical target? Given its ubiquitous expression, the severity of the phenotype seen in human and murine FTO deficiency, and the fact that adult deletion of FTO results in a dramatic loss of muscle mass, we believe it is unlikely. However, the understanding of FTO biology could potentially reveal novel therapeutic targets in our battle against the increasing epidemic of obesity. We also believe that the efforts to date in turning the statistical association of FTO with BMI into a deeper understanding of its biology and could form a template into how we approach the many other emerging GWAS obesity genes of unknown function.
