To unravel the mechanism regulating CD133 expression, we first screened small molecules including mTOR inhibitor (rapamycin), IκBα inhibitor (Bay 11-7082), Histone deacetylase (HDAC) inhibitors (apicidin, trichostatin A (TSA), and suberoylanilide hydroxamic acid (SAHA)), clinical anti-cancer agents (Doxorubicin (Dox) and 5-fluorouracil (5-FU)), and an inhibitor of microtubule formation (vincristine) on CD133 expression in human embryonic carcinoma NTERA2 cells. The gene discussed is PROM1; the disease is embryonal carcinoma.