It is important to note that targeting the Btk SH2-KD interface leads to particularly strong effects in DLBCL cell lines harboring CD79B ITAM mutations (Y196F in HBL-1 and Y196H in TMD8 cells) that trigger chronic activation of BCR, and are therefore heavily dependent on Btk signaling to support cell growth. Here, BTK is linked to diffuse large B-cell lymphoma.