It was not until 2011 that Zaugg et al. first revealed that CPT1C could inhibit the mTOR pathway and tumor reactivity to rapamycin in human breast cancer and lung cancer, and under external regulatory stimuli, such as reducing glucose concentration or a low-oxygen environment, CPT1C protein expression level could be promoted in an AMPKα-dependent manner and apoptosis could be inhibited, whereas knockdown of CPT1C was able to delay breast and colon cancer-derived tumor growth and metformin responsiveness in vivo [101]. This evidence concerns the gene CPT1C and breast carcinoma.