Since the loss of SBDS expression in healthy donor-derived cells is sufficient to reproduce the hyper-activation of mTOR-STAT3 signaling [26], we assume that alteration of the mTOR-STAT3-IL6 axis could be used by SDS cells as a survival mechanism that induces cell proliferation and myeloid growth in bone marrow, thus trying to escape from incoming neutropenia/aplasia processes. This evidence concerns the gene SBDS and Decreased total neutrophil count.