The effect of increased BCAT1 expression on glioblastoma cell proliferation was suggested to result from increased production of BCKAs, from the corresponding BCAAs, and their oxidation in the TCA cycle.7 However, inhibition of A11 cell proliferation by BCAT1 knockdown was not relieved by addition of BCKAs (Figure 5A). The gene discussed is BCAT1; the disease is glioblastoma.