Di Claudio, in his thesis about endometriosis, also showed the possibility of identifying potentially ‘high-risk’ patients who present a significant upregulation of genes involved in reprogramming (e.g., SOX2, NANOG), cancer metabolism (e.g., TP53, KRAS), and epithelial–mesenchymal transition (e.g., TGF alpha and SNA11). This evidence concerns the gene NANOG and endometriosis.