They can be categorized into five main subgroups: gain-of-function mutations in CRLF2; mutations conferring JAK1 function (typically associated with T-ALL); mutations conferring JAK2 function; mutations activating the extracellular domains of IL-7Rα, leading to heterodimer formation with CRLF2; and mutations in the transmembrane domain of IL-7Rα, resulting in ligand-independent homodimerization [65]. Here, CRLF2 is linked to acute lymphoblastic leukemia.