While most studies investigating the PRA- and PRB-dependent gene expression patterns were based on cell lines modified to synthesize only one isoform, providing insight to the genomic action of the homodimer forms alone, a research by Khan et al. compared gene expression in PRA(+)PRB(−), PRA(−)PRB(+) and PRA(+)PRB(+) breast cancer cells showing that indeed a certain subset of genes is regulated exclusively by the PRA-PRB heterodimer [87]. This evidence concerns the gene S100A6 and breast cancer.