It is probably that, in doxorubicin-resistant breast cancer cells, loss of the pioneer TF FOXA1 leads to a significant decrease in chromatin openness, which impairs the ability of co-regulators GATA3 and/or GRHL2 to occupy their specific binding sites in the promoter and/or enhancer region of specific genes, such as BATF, SLC44A2, and GPNMB. Besides, the opposite changes in gene expression of FOXA1 and GSTP1 might be potential therapeutic targets for overcoming or reversing doxorubicin resistance in breast cancer. This evidence concerns the gene GPNMB and breast carcinoma.