When the tumorspheres derived from MCF7 and T47D cells were treated with MG132, a proteasome inhibitor, the steady state level of ER-α66 protein was dramatically increased in both parental cells and tumorshphere cells (Figure 7B), suggesting that degradation of ER-α66 protein by the proteasome system is involved in regulation of the steady state levels of ER-α66, which was enhanced in ER-positive breast cancer stem/progenitor cells. This evidence concerns the gene ESR1 and breast carcinoma.