As constitutive IGF-1/IGF-1 receptor (IGF-1R) signaling contributes to deregulated PI3K activity and overexpression of IGF-1R was observed in malignant clonal cells in bone marrow of MDS in previous studies (35,36), the effects of exogenous IGF-1 stimulation on BIIB021-mediated inhibition of the PI3K/Akt signaling pathways were tested in the present study. Here, PIK3CD is linked to myelodysplastic syndrome.