Specifically, in a model of Type A HE, FXR expression has been shown to increase in neurons of the frontal cortex [19] and that intracranial infusion of an FXR-specific vivo morpholino to knockdown the expression of FXR attenuated the cognitive deficits observed in this HE model [19], suggesting that aberrant FXR signaling maybe contributing to the pathogenesis of HE. The gene discussed is NR1H4; the disease is hereditary elliptocytosis.