CD19 and precursor B-cell acute lymphoblastic leukemia: In following studies aimed to explore the mechanism associated with the CD19-/r B-ALL, in a cohort study of 12 patients with B-ALL, antigen loss was originated from alterations in CD19 exons 2–5 lead to a truncated protein with a nonfunctional or absent transmembrane domain, whereas alternatively spliced variants were found only with low frequency [40].