As increased TAL1 oncogenic activity was also evident in the accelerated cell growth observed after CRISPR knock-out of half of the USP7 loci in T-ALL cell lines, we hypothesize that USP7 haploinsufficiency in T-ALL down-regulates the ability of this deubiquitylating enzyme to remove ubiquitin from E-proteins, leads to enhanced TAL1 heterodimer formation, which favors TAL1-mediated thymocyte transformation. This evidence concerns the gene USP7 and acute lymphoblastic leukemia.