In conclusion we have shown that MHC-I gene expression is regulated by DNMT1 in human and mouse neuroblastoma cell lines, and that the gene expression of some but not all H2 subtypes is upregulated in post-mitotic CGNs upon knockdown of DNMT1. We moreover show that IFNγ can act in synergy with these treatments to further increase H2-D1/L gene expression. The gene discussed is IFNG; the disease is neuroblastoma.