Based on these data, we proposed that given HIF1α expression is induced under hypoxic conditions, deficient PB1 not only activates AKT–mTOR and the glycolysis signalling pathways but also exerts a synergetic effect on HI1a expression, which collectively promote ccRCC tumour growth (Figure 7D). This evidence concerns the gene AKT1 and nonpapillary renal cell carcinoma.