Although these observations are contrasting with regard to the specific Notch degradation mechanism along the endocytic route and lysosome compartment, and further studies are thus obviously required, HDAC6 inhibition through tubacin and its genetic silencing in T-ALL PDX models demonstrated an interplay between HDAC6 and the endocytic/lysosomal pathway and, furthermore, the antineoplastic effects of HDAC6 blockage [154]. The gene discussed is HDAC6; the disease is acute lymphoblastic leukemia.