A mutation in MYD88 (L265P) supports the survival of lymphoplasmacytic cells by activation of Bruton tyrosine kinase in Waldenström macroglobulinemia

Key Points MYD88 L265P is a widely expressed somatic mutation in WM patients that supports NF-κB signaling through stimulation of BTK and IRAK 1/4. Combined suppression of BTK and IRAK in MYD88 L265P expressing WM cells promotes synergistic inhibition of NF-κB signaling and WM cell killing.