In addition, REST was also reported to be regulated by RA through a posttranscriptional mechanism mediated by proteasomal degradation51, and RA can upregulate the expression level of REST-specific E3-ligase (Skp1-Cul1-F-box protein complex containing the F-box protein β-TRCP, SCFβ-TRCP), which promote REST proteasomal degradation in neuroblastoma cells12,51. This evidence concerns the gene REST and neuroblastoma.