Accumulation of N-tr-Aβ—unmodified and pyroglutamate-11 modified—in the prefrontal cortex in autism is mainly associated with the PVA+ GABAergic neurons, and the high load of N-tr-Aβ is correlated with lower levels of GAD67 (Frackowiak et al., 2020). The gene discussed is GAD1; the disease is autism.