In addition, under hypoxic conditions, PPAR γ-dependent hypoxia-inducible factor 1α (HIF-1α) exacerbated the autophagic phenotype of tumor stromal cells, and the HIF1α-PPARγ-UCP2-AMPK pathway significantly affected the mitochondrial biological function of CAFs, resulting in the metabolic reprogramming of CAFs and exacerbating breast cancer growth (Boutoual et al., 2018; Wang et al., 2019). The gene discussed is HIF1A; the disease is breast cancer.