Our data demonstrated that a large proportion of the predicted target DEGs were potentially co-regulated by both FOXA1 and GRHL2 in MCF7 cells (Figure 6E), such as SLC44A2, GPNMB, BATF, and GOLT1A, which suggested that loss of FOXA1/GRHL2 collaboration might be responsible for the down-regulation of critical genes in doxorubicin-resistant breast cancer cells. The gene discussed is FOXA1; the disease is breast carcinoma.