Because the TAZ promotor is epigenetically silenced in CML cells prior to the acquisition of drug resistance (Fig. 2I), we hypothesized that FLT3-induced TAZ-TEAD may deliver a distinct transcriptional output in hematologic malignancies compared to that of adherent cells, which constitutively express TAZ protein (Fig. S2B). Here, WWTR1 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.