Anergic CLL cells from TCL1 mice with regular NFAT2 expression showed evidence of constitutive activation of ERK1/2 as it is the case in the human disease11, whereas in CLL cells from TCL1 Nfat2−/− mice ERK1/2 was completely inactive without BCR stimulation and changed its activation status only after αIgM treatment. Here, NFATC1 is linked to B-cell chronic lymphocytic leukemia.