Given that expression of the nuclear PR variants A and B is induced by estrogens, which have been shown to exert distinct effects on breast cancer cells, data indicating that specific activation of PR variants increases the expression of cell-cycle-promoting genes, but represses growth inhibitory genes in breast cancer cells, might provide a plausible molecular mechanism underlying the elevated effect of EPT on breast cancer development [34]. This evidence concerns the gene PGR and breast carcinoma.