A significant proportion of AKT-S CLL cases (70%) responded to anti-IgM by activation of the BTK/PI3K/AKT axis, whilst only a small proportion of p38MAPK-S cases responded to anti-IgM by increasing the phosphorylation of p38MAPK (Porakishvili et al. 2015). This evidence concerns the gene BTK and B-cell chronic lymphocytic leukemia.