This allelic splice variant of HMSD is the precursor of the histocompatibility antigen ACC-6. More generally, minor histocompatibility antigens (mHags) refer to immunogenic peptide which, when complexed with MHC, can generate an immune response after recognition by specific T-cells. The peptides are derived from polymorphic intracellular proteins, which are cleaved by normal pathways of antigen processing. The binding of these peptides to MHC class I or class II molecules and its expression on the cell surface can stimulate T-cell responses and thereby trigger graft rejection or graft-versus-host disease (GVHD) after hematopoietic stem cell transplantation from HLA-identical sibling donor. GVHD is a frequent complication after bone marrow transplantation (BMT), due to mismatch of minor histocompatibility antigen in HLA-matched sibling marrow transplants. However, associated with GVHD, a favorable graft-versus-leukemia (GVL) can be induced by donor-recipient disparities in mHags. ACC-6 is presented to the cell surface by MHC HLA-B*4403. This complex specifically elicits donor-cytotoxic T-lymphocyte (CTL) reactivity against hematologic malignancies after treatment by HLA-identical allogenic BMT. It induces cell recognition and lysis by CTL. Immunogenicity of most autosomal mHags results from single-nucleotide polymorphisms that cause amino-acid substitutions within epitopes, leading to the differential recognition of peptides between donor and recipient. ACC-6 forms a complex with MHC HLA-B*4403. Highly expressed in dendritic cells and primary leukemia cells, especially those of myeloid lineage. ACC-6 expression is limited to cells of the hematopoietic lineage. Minor histocompatibility antigen ACC-6 (mHA ACC-6) is encoded by HMSD-v which is an allelic variant of HMSD. HMSD-v results from an intronic single-nucleotide polymorphism located at position 5 of HMSD intron 2 leading to a G to A substitution. This variation in intron 2 induces skipping of exon 2 and frameshift, resulting in expression of ACC-6. This alternative splicing event arises as a consequence of an intronic polymorphism. Translation of HMSD-v form generating mHA ACC-6 is in a frame different from that resulting in HMSD non variant form expression. Thus, the HMSD non variant form sequence does not contain the mHA ACC-6 peptide.