Patient-derived cell lines and primary samples were used in both <i>in vitro</i> and <i>in vivo</i> experiments to model Waldenström's macroglobulinemia and its response to IRAK1/4 inhibitors.
The results establish BTK as a downstream target of MYD88 L265P signaling, and provide a framework for the study of BTK inhibitors alone, and in combination with IRAK inhibitors for the treatment of WM.