Moreover, we showed using ChIP–quantitative polymerase chain reaction (qPCR) that exogenous expression of RB1 in C33A cells decreased interaction of ESRRG with promoters of canonical ESRRG-regulated genes (SDHD, IDH3A, and ATP5G3) (20, 21), whereas knockout (KO) of RB1 in RB1-WT SH-SY5Y neuroblastoma cells resulted in increased ESRRG interaction with these promoters (Fig. 4E and fig. The gene discussed is ESRRG; the disease is neuroblastoma.