Herein we focus on PKC and GSK3 because (a) they have been shown to play a key role in regulating the level of expression and the entry into the nucleus of Nrf2 itself, and, in addition, in an opposite manner, as described below, and (b) their level of activity is dysregulated in CLL, which makes it reasonable to infer that the activation status of these protein kinases themselves can affect Nrf2 signaling. This evidence concerns the gene PRRT2 and B-cell chronic lymphocytic leukemia.