In conclusion, multiple receptors and signal transduction cascades influence T-cell function and fate. During the past few years many of these important aspects of T-cell biology were identified. The complexity of the various signaling pathways has made appreciation of their clinical significance difficult. One way of studying the function of these molecules is to create mice deficient of these components. However, frequently the murine phenotype is far from reflecting the homologous human deficiency. It is therefore beneficial to define the human immunodeficiencies in order to understand the role of a certain signaling molecule in humans. Further, mutations that result in partial deficiencies may result in a different phenotype from null mutations. This information may aid in improving structure/function analysis of these signaling components.