Following evidence that activated β-catenin signaling in the BM niche is a driving force of myeloid neoplasms [40], the antihelminthic drug pyrvinium was used to inhibit increased microenvironmental β-catenin signaling in the adenomatous polyposis coli (APC) haploinsufficiency mouse model of MDS [72]. This evidence concerns the gene APC and myeloid neoplasm.