This resistance results from the activation and recruitment of WNT signaling constituents to compensate for BRD4 loss, a mechanism defined as “transcriptional plasticity.” In contradiction to the earlier findings that loss of PRC2 sensitizes brain tumor cells to BET inhibitors, ten-eleven translocation 2 (TET2), a dioxygenase, catalyzes DNA demethylation. The gene discussed is TET2; the disease is brain neoplasm.