Although unique variants were observed in the EPCAM+CD44+CD49f+ cells, these may correspond to a quiescent subpopulation of cancer initiating cells or represent de novo acquired mutations that have yet to populate the bulk tumor, as enrichment of the EPCAM+CD44+CD49f+ subpopulation may have uncovered variants that could be present in low frequency in the bulk tumor, but at higher frequency with respect to the cancer initiating cell subpopulation. This evidence concerns the gene EPCAM and neoplasm.