Interestingly, Chi et al. found that high expression of BCAAs in breast tumor tissues can reduce breast cancer N-cadherin’s expression level and thus inhibit tumor metastasis.59 Shafei reported that BCAT1 inhibited the Ras/ERK pathway and activates PI3K/AKT pathway through insulin/IGF-1, ultimately promoting the expression levels of FOXO3a and Nrf2 and regulating the proliferation, migration, and invasion in triple-negative breast cancer (TNBC).55 The above studies imply that breast cancers can be classified into subtypes based on their preference for BCAAs metabolism. This evidence concerns the gene BCAT1 and neoplasm.