Efforts to detect these “bad actors” have included the exploitation of various properties of CTCs that are either independent or less reliant on their EMT status (e.g., size/deformability [microfiltration/microfluidics], electrical properties [dielectrophoresis], immunomagenetic approaches using organ/tumor specific-antigens [carcinoembyronic antigen (CEA), epidermal growth factor receptor (EGFR), prostate specific antigen (PSA), mucin-1 (MUC-1)], and adhesion assays based on CTCs ability to adhere to the presented capture surface) [35]. This evidence concerns the gene MUC1 and neoplasm.