In concordance with the genomic observation that majority of PHF6 somatic mutations are presumed loss-of-function frameshift and nonsense mutations, multiple mouse studies have reported increased HSC self-renewal with Phf6 knockout [17–19, 27], and have reported enhanced T-ALL progression when Phf6 knockout is combined with activating mutations in Notch1 or Jak3, or overexpression of Tlx3 [17, 18, 20]. The gene discussed is JAK3; the disease is acute lymphoblastic leukemia.