In vivo treatments, including the FOLFOXIRI regimen or irinotecan, and in vitro treatment comprising 5-Fluorouracil (5-FU), OXA, and camptothecin can promote the hydrolysis of type XVII collagen (COL17A1) (a cell-adhesion molecule that strengthens hemidesmosomes) and activate the FAK-YAP pathway, thereby prompting dormant LGR5p27 cancer cells to re-enter the cell cycle. Here, PTK2 is linked to cancer.