Based on the ChIP-seq data from primary human ST-EPN-YAP1 specimens (cf. Fig. 5) and nuclear accumulation of the YAP1-MAMLD1 protein in human primary tumors (Fig. 1e–g), we hypothesized that the transcriptional programme of YAP1 fusion-driven ependymoma is dependent on direct interaction between the fusion and TEAD TFs. The gene discussed is MME; the disease is ependymoma.