The majority of neuronal cell models commonly used for such studies include wild-type neuroblastoma cell lines or primary rodent neurons where GCase enzyme activity or GBA1 expression levels are exogenously modulated by treatment with the GCase suicide inhibitor conduritol B epoxide (CBE) (Manning-Bog et al., 2009; Cleeter et al., 2013; Dermentzaki et al., 2013), transfection with GBA1-specific siRNAs (Mazzulli et al., 2011), or over-expression of plasmids containing mutant GBA1 (Cullen et al., 2011). This evidence concerns the gene GBA1 and neuroblastoma.