S1g-2 and S1g-6 significantly inhibited the growth of chronic myeloid leukemia in vitro and in vivo, and more importantly, S1g-2 exhibited an ever-growing ability to induce apoptosis and increase BCR-ABL independent TKI resistance in chronic myeloid leukemia cells [104,105,106]. This evidence concerns the gene BCR and chronic myelogenous leukemia, BCR-ABL1 positive.