Increased BCAAs and FAs levels (Fig. 10a–d) were a consequence of ECHS1 inactivation; increase in the levels of phospho-4EBP, readout of mTOR signaling activation and BCAAs accumulation; higher BCL2 levels, a signature of apoptosis resistance, were all increased in fresh tissue samples of RCC and HCC (Fig. 10a, b, Supplementary Figs. 16–21). The gene discussed is BCL2; the disease is hepatocellular carcinoma.