In contrast, in the ER-negative basal-like breast cancer cells, EZH2 interacts with RelA and RelB (Figure 3a and Table 2), two core subunits of NF-κB, and functions as NF-κB coactivator independent of its histone methyltransferase activity [70]; this role of EZH2 in promoting NF-κB signaling was in agreement with the EZH2-mediated transcriptional activation of RelB, again through a methyltransferase-independent mechanism, to sustain the self-renewal and tumor-initiating phenotypes of TNBC cells [30]. Here, RELB is linked to breast carcinoma.