Up until recently, the idea of CPV against non-viral cancers has been associated with a high risk of autoimmunity because in the vast majority of clinical trials the targeted antigens were TAAs, which generally derive from self-antigens that are selectively or over-expressed in tumor cells or involved in tissue differentiation such as the transmembrane glycoprotein Mucin 1 (MUC1) [20]. This evidence concerns the gene MUC1 and neoplasm.