GAD2 and epilepsy: We therefore hypothesized that loss of 5-HT2C receptors that activate GABAergic neurons provides a parsimonious explanation for epilepsy and SUDEP in loxTB Htr2c mice, however, in the Gad2Cre-Htr2c model with selective expression only in Gad2+ interneurons, we observed identical EEG abnormalities and spontaneous seizures, and premature mortality was increased rather than blunted (Fig. 5C).