For instance, a cell-penetrating fused protein construct, TAT-ODD-p53, which consists of a TAT domain of human immunodeficiency virus-1, oxygen-dependent degradation domain (ODD) of HIF-1α and wild-type p53 was shown to selectively accumulate in hypoxic breast cancer cells and render them more radiosensitive by inhibiting the autophagic digestion of the mitochondria (mitophagy) [252]. The gene discussed is HIF1A; the disease is breast carcinoma.