While loss of both BCAT1 and BCAT2 has been associated with impaired NSCLC tumor formation but no effect on pancreatic ductal adenocarcinoma (PDAC) 11, increasing expression of BCAT2 facilitated BCAA uptake and sustained mitochondrial respiration in PDAC 48. Here, BCAT1 is linked to pancreatic ductal adenocarcinoma.