It is known that 5–7% of patients with B-ALL show an overexpression of CRLF2 disrupting the JAK/STAT pathway, and this is commonly associated with activating JAK2 somatic mutations by rearrangements [12,43,50,51,52], rendering a possible therapeutic target for ruxolitinib, a JAK1/2 inhibitor. Here, JAK2 is linked to acute lymphoblastic leukemia.