The B-cell linker protein is encoded by the BLNK gene and is an adaptor protein also known as SLP-65, BASH, and BCA. BLNK is expressed in B cells and macrophages and plays a large role in B cell receptor signalling, in a fashion analogous to the role its paralogue SLP-76 plays in T cell receptor signalling. As it has no known intrinsic enzymatic activity, the function of BLNK is to temporally and spatially coordinate and regulate signalling effectors downstream of the B cell receptor. The function of BLNK was first illustrated in BLNK deficient DT40 cells, a chicken B-cell line, which exhibited an abrogated intracellular calcium mobilisation response and impaired activation of MAP kinases p38, JNK, and to a lesser degree ERK upon B-cell receptor (BCR) activation as compared to wild type DT40 cells. In knockout mice, BLNK deficiency results in a partial block in B-cell development, and in humans BLNK deficiency results in a much more profound block in B-cell development. Linker or adaptor proteins provide mechanisms by which receptors can amplify and regulate downstream effector proteins. The B-cell linker protein is essential for normal B-cell development.