Signal transduction by the BCR is critical for progression through developm
ental checkpoints as well as for immune responses. Recent results obtained
in mice deficient either in an adaptor molecule, BLNK (alternatively named
SLP-65 or BASH), or in phosphatidylinositol 3-kinase have revealed similar
- though not identical - phenotypes to those of Btk(-/-) mice, suggesting a
functional link between BLNK, Btk and phosphatidylinositol 3-kinase.