Elzinga et al. found that autophagy was required for the decline of BCR-ABL protein and that siRNA-mediated knockdown of autophagy regulators (Beclin 1/ATG7) as well as the pharmacological inhibition (3-MA) of autophagy reduced BCR-ABL/LC3 co-localization in both K562 and CML patient cells [201]. This evidence concerns the gene BCR and chronic myelogenous leukemia, BCR-ABL1 positive.