This finding was further supported in our BCAA catabolic inhibitory models, which demonstrated that knockdown of BCAT1 could successfully reduce lipid content in LNCaP and PC3 cells, while knockdown of BCAT2 results in an increase to lipid content in PCa cells, but not in benign BPH-1 cells. This evidence concerns the gene BCAT1 and benign prostatic hyperplasia.