This synucleinopathy model harnesses the Ca2+/calmodulin-dependent kinase II (CaMKII)–tTA promoter to drive human α-syn A53T (Lin et al., 2009), leading to high expression levels in the cerebral cortex, a region significantly affected in DLB and PD (Alafuzoff and Hartikainen, 2017). This evidence concerns the gene CAMK2G and synucleinopathy.