Suppl. Fig.1 KEGG B-cell receptor signaling pathway. Added by YLW.

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Suppl. Fig.1 KEGG B-cell receptor signaling pathway. Added by YLW

NTScrsiBTKNTScrsiBTK CLL162CLL239 BTK GAPDH Suppl. Fig.2. Genetic knock-down of BTK. A. Knock-down of BTK with siRNA was initially validated by immunoblotting in primary CLL cases (CLL162 and CLL239). NT, no treatment; Scr, scrambled siRNA control. siBTK, siRNA specific for BTK. B. A flow cytometric assay was later validated against Immunoblotting to determine the levels of total BTK protein. The assay was used in this particular patient, CLL015, to assess the BTK knockdown efficiency for the proliferation assay shown in Fig. 4A. Iso, isotype control. Scr, scrambled siRNA control. siBTK, siRNA specific for BTK. Iso scr siBTK Cell Number Total-BTK CLL015 A B

3 WT Mutant Suppl. Fig.3. Structural modeling of dasatinib in complex with WT BTK or BTK C481S.

4 18.7% 7.05% 8.12% 4.25% 0.36% No drug 250nM ibrutinib 250nM Idelalisib 1000nM Idelalisib 5000nM Idelalisib 7-AAD BrdU Suppl. Fig.4. Idelalisib has the potential to overcome ibrutinib resistance. Ibrutinib-resistant Relapsed s1 specimen was tested against varying doses of idelalicib (C max : ~6  M). Left panel, percentages of BrdU + CLL cells. Treatment conditions were indicated. Right panel, proliferation rates (%) were normalized to no drug control (100%). 100 Normalized Proliferate Rate (%) no drug 1.9% 37.7% 250nM ibrutinib 250nM1000nM5000nM 43.4% 22.7% idelalicib