Similarly, Notch pathway inhibition by the deletion of the ubiquitin E3 ligase Mind bomb 1 (Mib1) under two independent promoters (MMTV and Mx1) resulted in a non-transplantable myeloproliferative neoplasm-like disease, which could be reversed by activation of Notch in the microenvironment (MMTV-Cre;Mib1flf) [55], and deletion of Dicer1 in mesenchymal osteoprogenitors induced disordered haematopoiesis affecting multiple lineages, recapitulating key features of AML and myelodysplastic syndrome (MDS), and were microenvironment dependent [56]. This evidence concerns the gene MX1 and myelodysplastic syndrome.