Recent studies have shown that T-ALL results from multistep transformation processes that involve the accumulation of genetic defects, including activating mutations of NOTCH1 or JAK-STAT, super-enhancer generating mutations of TAL1, deep deletion of cell cycle-related genes (such as CDKN2, RB1, and CDKN1B), and inactivating mutations of WT1, LEF1, GATA3, and PHF6 [4–6]. Here, PHF6 is linked to acute lymphoblastic leukemia.