Conversely, overexpression of CHCHD4 in tumour cells was shown to increase basal cellular OCR and intracellular hypoxia [83], and led to enhanced HIF-1α stabilisation in hypoxia [16], all of which were blocked by the CIV inhibitor sodium azide [16,83] (Figures 2, 3). This evidence concerns the gene CHCHD4 and neoplasm.