Efficacy of SYK-inhibitor fostamatinib to suppress α-BCR–induced signaling depends on BCR signaling strength in MCL tumors. Samples from 13 MCL patients were left untreated or were treated with the SYK-inhibitor fostamatinib (SYK-i, 2.5 μM) for 1 hour, prior to α-BCR stimulation for 4 minutes. The cells were stained with lineage-specific markers and phosphospecific Abs as earlier described. (A) Histogram overlays of p-SYK, p-BTK, p-PLCγ, and p-AKT for lymphoma cells treated with fostamatinib, α-IgM or α-IgM + fostamatinib, relative to unstimulated (untreated) cells. (B) Scatter plots of α-IgM–induced phosphorylation vs percentage of fostamatinib suppression of α-IgM–induced phosphorylation levels for SYK, PLCγ, BTK (Y223), and AKT. Each dot represents a MCL patient sample (n = 13). Correlations were calculated by the Spearman rank test.