This finding reaffirms that while obesity renders most leptin-responsive neurons insensitive, those neurons involved in autonomic control are spared or even sensitized, “selective leptin resistance.” This result also indicates that it will be challenging to identify specific cellular mechanisms of sensitization, because the autonomic population of neurons in the ArcN (and other sites) is such a small fraction of all neurons containing LepR/InsR or influenced indirectly by leptin or insulin. The gene discussed is INS; the disease is obesity disorder.