CRLF2 and acute lymphoblastic leukemia: Molecularly, the vast majority, if not all cases of Ph-like ALL, harbor alterations in genes conferring de-regulated kinase-activity; in particular, translocations involving the CRLF2 gene are observed in about half of the cases and generate fusion proteins or lead to increased CRLF2 expression driven by the immunoglobulin heavy-chain (IgH) enhancer [12].