Consistent with our discovery using genetic silencing and PROTAC-mediated protein degradation approaches, a study published during our revisions revealed that treating NB cells with BRM014, an ATPase inhibitor of SMARCA4 and SMARCA2, also reduces the binding of core TFs to genomic loci with decreased chromatin accessibility (Cermakova et al, 2024). The gene discussed is SMARCA4; the disease is neuroblastoma.