Mutated (M)-CLL cells were found to be more sensitive towards apoptosis after treatment with TLR ligands in contrast to unmutated (UM)-CLL [43]. However, subsequent studies uncovered paradoxical detrimental results of TLR1/2/6 resulted in survival of CLL leukemic cells through nuclear factor kappa-B (NF-κB) signaling [44]. In a similar manner, treatment of CLL cells with TLR7 and TLR9 agonists promoted their clonal expansion [45]. The gene discussed is TLR1; the disease is B-cell chronic lymphocytic leukemia.