To determine if the alternative, low-abundance, in-frame transcript could drive CRLF2 overexpression and, in turn, potentially contribute to the biology of ALL driven by P2RY8-CRLF2 fusions, we cloned the canonical and alternative version of the P2RY8-CRLF2 fusion, as well as a frameshift version to act as a negative control, into retroviral vectors. The gene discussed is CRLF2; the disease is acute lymphoblastic leukemia.