CD79A is an essential component of the B-cell antigen receptor (BCR) complex that initiates signal transduction cascades upon antigen binding 1. Working cooperatively with CD79B, CD79A is required for BCR surface expression, internalization, trafficking to late endosomes, and antigen presentation [UniProt]. The protein stimulates SYK autophosphorylation and binds BLNK, facilitating SYK-mediated phosphorylation and B-cell activation [UniProt]. CD79A serves as a critical B-cell marker in immunohistochemistry, particularly useful for diagnosing B-cell neoplasms and precursor B-acute lymphoblastic leukemia when other markers like CD20 are absent 2. In disease, CD79A mutations are frequently detected in activated B-cell-like (ABC) diffuse large B-cell lymphoma (DLBCL), occurring in approximately 18% of cases 1. These mutations in the ITAM signaling modules increase surface BCR expression and attenuate negative feedback inhibition, promoting chr19 active BCR signaling essential for ABC DLBCL survival 1. This dependency on BCR signaling in ABC DLBCL makes CD79A/CD79B-targeted therapies clinically significant 3. Additionally, CD79B surface expression levels—regulated by KLHL6-mediated degradation—determine sensitivity to polatuzumab vedotin, a CD79B-targeting antibody-drug conjugate approved for first-line DLBCL therapy 4. Germline CD79A mutations cause autosomal recessive agammaglobulinemia [UniProt], highlighting its critical developmental role in B-cell differentiation.