For example, CLL patients who relapse after ibrutinib acquire mutations in Bruton Tyrosine Kinase (BTK) or phospholipase C-γ2 (PLCγ2) [45], whereas ibrutinib refractory MCL patients acquire mutations within several pathways, including genes of the NF-kB pathway, the mTOR pathway, and epigenetic modifiers [46]. This evidence concerns the gene MTOR and B-cell chronic lymphocytic leukemia.