We had originally hypothesized that CD22ΔΕ12 might act as an oncogenic protein by competitively binding to the cis ligands of CD22 and preventing residual wildtype CD22 from in cis ligand binding, thereby contributing to the increased proliferation and defective apoptosis of leukemic B-cell precursors from B-ALL patients caused by the CD22ΔE12-associated impaired regulatory function of CD22 [7,8]. Here, CD22 is linked to acute lymphoblastic leukemia.