Alternatively, reduced VGCC expression in juvenile and adult FMR1 KO animals could be a compensatory change, as it has been shown that there is increased Ca2+ influx through L-type VGCCs in neural progenitor cells from FMR1 KO mice and FXS human-derived pluripotent stem (iPS) cells (Danesi et al., 2018). This evidence concerns the gene FMR1 and fragile X syndrome.