To ascertain the role of endogenous HIF-1α accumulation during CCH in rats, we used a loss of function approach by silencing HIF-1α expression using lentivirus-mediated shRNAi (short-hairpin RNA interference) against HIF-1α mRNA (pLVx-GFP-shHIF-1α). The gene discussed is HIF1A; the disease is columnar cell hyperplasia of the breast.