The proof of concept studies using structurally stable, resistant to nucleases double-stranded LNA GapmeRs, e.g., against lnc-THADA4-1 in Juvenile Myelomonocytic Leukemia (JMML) [132], and antisense double-stranded DNA oligonucleotides (ADO) against BCR-ABL in CML [190], suggest that RNase H-mediated RNA degradation is a potentially effective therapeutic strategy, that requires further validation in vivo. This evidence concerns the gene ABL1 and juvenile myelomonocytic leukemia.