For PCC, chlorogenic acid effectively suppressed pancreatic ductal adenocarcinoma cell growth in vitro and in vivo by inducing mitochondrial respiration dysfunction and depressing cellular bioenergetics via modulating the MYC proto-oncogene, bHLH transcription factor-transferrin receptor 1 (c-Myc-TFR1) axis [273]. Here, TFRC is linked to pancreatic ductal adenocarcinoma.