In addition, several in vitro studies suggest that MDS-MSCs have impaired PI3K/AKT and Wnt/ß-catenin signaling (Pavlaki et al., 2014; Falconi et al., 2016) which may explain their abnormal proliferation, self-renewal, and osteogenic differentiation (Figure 2) (Boland et al., 2004; Glass et al., 2005). Here, AKT1 is linked to myelodysplastic syndrome.