It owns good oral tolerance and efficacy in the MMTV-Wnt1 mouse mammary cancer model,295 the Znrf3/Rnf43−/− mouse CRC model.284 And WNT-C59 satisfactorily prevented tumor growth in mice xenografted with SUNE1 or HNE1 (two nasopharyngeal carcinoma cell lines).296 In addition, WNT-C59 can reverse the resistance of trichostatin A in human pancreatic cells.297 However, when administrated at 10 mg/kg/d for 7 or 21 days, bone loss was observed in mice.281 This should be taken into consideration as the potential side effect of WNT-C59 in cancer therapies. This evidence concerns the gene WNT1 and cancer.