DNMT3A and neoplasm: A recent study found that the 5‐methylcytosine dioxygenase TET1 interacts with TEAD to cause regional DNA demethylation in YAP target genes, facilitating transcriptional activation in hepatomegaly and tumorigenesis.[29] Based on our findings, YAP/TAZ cooperates with DNA methylation to facilitate tumor malignancy in two ways: by interacting with the DNA methyltransferase DNMT3A to induce DNA methylation‐mediated transcriptional repression of tumor suppressor genes, and by interacting with the DNA demethylase TET1 to eliminate DNA methylation and activate oncogenes.