Also, despite the low incidence of MYD88/TLR pathway mutations in CLL, TLR pathway inhibition is a viable therapeutic strategy for CLL as preclinical data has shown that inhibition of IRAK-4 with a competitive IRAK-4 inhibitor (ND2158) decreased the viability and proliferation in patient-derived CLL cells, including those that did not harbor MYD88L265P mutations suggesting that IRAK-4 promotes tumorigenesis independent of MYD88L265P mutation (46, 47). Here, IRAK4 is linked to B-cell chronic lymphocytic leukemia.