BCR and acute lymphoblastic leukemia: The genetic deficiency of aPKCλ or both aPKCζ and -λ, but not aPKCζ alone, or the pharmacological inhibition of aPKCs, attenuate the development of a p210-BCR-ABL- or TKI-resistant p210-BCR-ABL-induced human and murine CML-like disease, and completely abrogate the progression to B-ALL.