Previous studies have demonstrated that loss of TFAP2C expression induced EMT in luminal breast cancers [9] and recent findings confirm a role of TFAP2C in regulating EMT in lung cancer [35]; furthermore, inhibiting sumoylation of TFAP2A activated a transcriptional program replicating TFAP2C functionality that induced mesenchymal-epithelial transition (MET) in basal breast cancer [10]. This evidence concerns the gene TFAP2C and lung carcinoma.