Importantly, S1g-2 exhibited high apoptosis-inducing activity in chronic myeloid leukemia (CML) cells, making it a completely new class of HSP70 inhibitory strategy.581 Subsequently, S1g-10 was yielded by optimizing S1g-2, exhibiting a 10-folds increase in HSP70-BIM PPIs suppressing potency.582 Besides, the binding mechanism of the class inhibitors was further explored based on another S1g-2 derivative, S1g-6. This evidence concerns the gene HSPA1A and chronic myelogenous leukemia, BCR-ABL1 positive.