By contrast, a significant number of achondroplasia patients that carry activating FGFR3 mutations also manifest atypical obesity.55 Difficulties that prevent drawing firm conclusions from human patients include: the germline nature of these mutations, which would additionally impact peripheral organs or indeed multiple brain regions; their rareness, which may preclude statistically valid associations with metabolic/neuroendocrine defects or diet; and their varied molecular mode of function, with some mutant receptors operating in a FGF ligand‐independent manner. The gene discussed is FGFR3; the disease is achondroplasia.