PRNP and cancer: If the redox cycling between heme and hemin is intended as a natural feedback control for prion conversions, then the elevated ROS in TME together with increased oxidative stress from prolonged peroxidase activity from PrPC-hemin complexes [369,588] may terminate the feedback cycle to favor increased hemin-PrPC binding that heightens cancer drug resistance as a result of elevated hemoglobin synthesis.