Thus, these cell type-specific Stxbp1 heterozygous deletions did not recapitulate the full extent of neurological impairments in STXBP1 encephalopathy and constitutive Stxbp1 haploinsufficient mice, which seems to suggest that neither glutamatergic nor GABAergic/glycinergic neurons are critical for the disease pathogenesis. Here, STXBP1 is linked to Encephalopathy.