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MBL2 and fever during neutropenia in children with acute lymphoblastic leukaemia

negative clone, is an important observation that we believe has not been reported previously. Clinical studies that compared conventional chemotherapy without or with FLT3 inhibitor have yielded conflicting outcomes (Levis et al, 2011; Ravandi et al, 2010; Serve et al, 2010). The timing of of FLT3 inhibitor administration in relation to chemotherapy is probably a critical factor (Levis et al, 2004), where prior administration may inhibit the effects of subsequent chemotherapy (Pratz & Levis, 2008) while treatment following chemotherapy may be ineffective due to high circulating FLT3-ligand (Sato et al, 2011). In this regard, our observation of a sustainable suppression of the FLT3 clone by Sorafenib alone is especially informative as it suggests that FLT3 inhibitor has a definite and enduring role in complementing concomitant chemotherapy given for the FLT3-ITD wild type clones. Whether the adverse natural course associated with FLT3-positive AML could be altered with this strategy is worth exploring.