In this context, we suggest that the observed difference in SIN3A interaction with the CTTNBP2 CRE between SH-SY5Y and LAN-2 may be due to SIN3A’s role as a corepressor of REST in the repression of neuronal genes, potentially influencing CTTNBP2 gene repression specifically in MYCN non-amplified NB cells, such as SH-SY5Y, where this transcription factor is overexpressed [32–34]. The gene discussed is CTTNBP2; the disease is neuroblastoma.