So far, little is known about deregulated genes or pathways that could predispose patients to relapse; however, recently Perova et al. [5] reported the relevance of spleen tyrosine kinase (SYK) activation in sustaining the growth of multiple high-risk (HR) B-ALL subtypes, showing that SYK inhibitors, such as fostamatinib, potently reduce the disease burden in mice xenotransplant studies, suggesting that SYK inhibitors may improve the outcome for HR and relapsed B-ALL patients [5]. Here, SYK is linked to precursor B-cell acute lymphoblastic leukemia.