Activating mutation in MyD88 is shown to induce survival NFκB signaling pathway via IRAK1/IRAK4 or bruton tyrosine kinase (BTK) pathways and also increase transcription and activation of SRC family member, HCK, which in turn increases WM tumor cell growth and proliferation via BTK, AKT and ERK signaling pathways [14]. The gene discussed is NFKB1; the disease is neoplasm.