We show that the combination of these two agents in patient-derived ATRT cell lines leads to dramatic changes in gene expression, including activation of innate immune signaling via the STING/interferon pathways, upregulation of genes controlled by bivalent promoters or SMARCB1 expression, and re-expression of silenced tumor suppressors such as CDKN2A. This is accompanied by a synergistic reduction in cell viability. The gene discussed is CDKN2A; the disease is neoplasm.