Indeed, several Notch targets are also Pin1 substrates (for example, cyclone D1 and NF-kB).17 This may suggest that Pin1 could promote T-ALL aggressiveness also by enhancing the activity of some Notch3-induced Pin1 targets, such as the NF-kB transcription factor, we previously showed to be activated by Notch357 and known to be regulated by Pin1 isomerase also in leukemia/lymphoma development.58 In this way, Pin1 blocking may represent a new approach for targeting a common oncogenic mechanism to stop the multiple cancer-driving pathways, which act simultaneously in the disease. This evidence concerns the gene NFKB1 and acute lymphoblastic leukemia.