Activation of Akt was noted to occur more frequently in aggressive CLL.[37] We have previously reported the upregulation of mROTC1‐related proteins in CLL patients, especially those with refractory or relapsed disease.[38] With the treatment of the dual ATP‐competitive PI3K and mTOR inhibitor dactolisib, the proliferative ability of CLL cells was observed to be significantly impaired. Here, MTOR is linked to B-cell chronic lymphocytic leukemia.