We found a reciprocal expression of these T-box factors, with TBX3 downregulated in TBX2-expressing HC11 cells but upregulated in TBX2-depleted HC11+TBX2 and MDA-MB-435 tumor cells (Figure S5A, S5B), which is reminiscent of the mutually exclusive expression patterns of TBX2/3 in normal mammary gland tissues [23], [79], Thus, the TBX2-induced EMT phenotypes were not due to a possible interference by TBX3 but rather may reflect the poorly explored role of TBX2 as a mesenchymal and baso-myoepithelial transcription factor in breast development [23], [24]. Here, TBX2 is linked to neoplasm.