CASP3 and acute lymphoblastic leukemia: In contrast to our previous observation showing that TPGS-induced apoptosis in acute lymphoblastic leukemia (ALL) cells by at least 2 complementary death subroutines (i.e., p53-dependent: H2O2>NF-κB>p53>PUMA and p53-independent: H2O2>JNK>p-c-JUN>PUMA) that converged in mitochondrial damage, caspase activation, and nucleus fragmentation [17], TPGS induced cell death in K562 by a minimal mechanism involving an H2O2-dependent and p53-independent pathway, i.e., H2O2>JNK>p-c-JUN (Ser63/Ser73)>PUMA>ΔΨm (down)>caspase-3 (up)>dot-like/sphere-like shape DNA fragmentation (Figure 9).