Monogenic PD cases due to GBA1 loss of function and subsequent substrate accumulation have been investigated in cellular and animal models and in studies of human brains of patients with GBA1-associated PD showing to particularly affect pars compacta of SN, putamen, cerebellum, and amygdala and frontal cortex (Gegg et al., 2012; Moors et al., 2019). The gene discussed is GBA1; the disease is Parkinson disease.