Hence, the strong increase of STAT5 phosphorylation occurred already in early leukemogenesis concomitant with loss of the wild‐type Pax5 allele and increased DNA‐binding of Pax5‐Jak2, which provides compelling evidence for a nuclear function of Pax5‐Jak2 in maintaining high levels of p‐STAT5 in Pax5Jak2/+ B‐ALL cells. Here, STAT5A is linked to acute lymphoblastic leukemia.