The prevalence of the somatic MYD88 L265P mutation is over 90% in patients with Waldenstrom macroglobulinemia (WM), and the Bruton tyrosine kinase (BTK) pathway plays an essential role in the signaling of mutated MYD88 providing survival advantage and proapoptotic mechanisms to malignant WM cells [1]. This evidence concerns the gene BTK and Waldenstrom macroglobulinemia.