**1. Introduction**

The recognition specificity of different non–self-antigens or defective selfantigens (tumors) by a well-defined B-cell clone does not result from the presence of an extensive number of receptor genes, but rather from immunogenetic mechanisms affecting a limited number of IG genes, including mechanisms of genetic recombination, mutations, deletions or insertions, and gene repair, through very complex regulatory mechanisms that are responsible for a large B-cell repertoire.

This chapter focuses on the molecular description of the immunogenetic mechanisms responsible for the generation of B-cell antigen receptor diversity.
