In breast cancer, while direct evidence linking BCAA metabolism to TCA cycle metabolite levels is limited, inhibition of key enzymes such as BCAT1 and BCKDK has been shown to reduce both basal and maximal respiration, as well as ATP production, indicating a functional role for BCAA metabolism in supporting mitochondrial energy output [20,22,23]. The gene discussed is BCAT1; the disease is breast carcinoma.