We have proposed before that increased motor cortex excitability is a compensatory mechanism aiming to reduce thalamic overactivity and thus pain (Castillo Saavedra et al., 2014); though this mechanism is not enough to control pain (an anology here would be increased insulin in a subject with hyperglycemia; increased insulin levels would be the compensatory mechanism). The gene discussed is INS; the disease is Hyperglycemia.