A possible explanation for this may be that ALL and ML cells express the apoptosis inhibitor Bcl-2[46] and the endogenous inhibitor of granzyme B, proteinase inhibitor 9 (PI-9).[47], [48], [49], [50] The expression of these two factors by malignant lymphoid cells may protect them from granzyme B-induced apoptosis and proteolysis[46], [48] and might thus negate the differential effects of the different granzyme B genotypes. Here, BCL2 is linked to acute lymphoblastic leukemia.