The observed upregulation of complexin 1 protein in radioimmunoprecipitation assay (RIPA) buffer fractions of these cells after 2 days contrasts with the downregulation of complexin 1 protein in 8 M urea fractions that was recently observed in the prefrontal cortex of autopsied individuals who had PD in old age (Dumitriu et al., 2016) and might be explained by altered CPLX1 solubility, by progression from acute to chronic SNCA gain of function or by other differences between neuroblastoma cells versus cortical postmitotic neurons. Here, CPLX1 is linked to Parkinson disease.