It has been demonstrated that, in ccRCC, this condition can induce the stabilization of hypoxia-inducible factors-αs (HIF1α and 2α), which in turn can promote metabolic reprogramming, angiogenesis, and epithelial–mesenchymal transition (EMT) associated with the downregulation of tight junction protein (occludin, claudin-1, and E-cadherin) expression and apical–basal polarity loss. Here, HIF1A is linked to nonpapillary renal cell carcinoma.