ARID4B and neoplasm: Inhibiting BCAT1 is an attractive strategy because it can disrupt multiple pro-tumor processes at once: it slows BCAA catabolism (potentially starving the TCA cycle), it may cause toxic buildup of BCKAs, it reduces glutamate production (impacting redox balance and nucleotide synthesis), and it can restore normal α-KG levels (thereby potentially reversing certain epigenetic changes).