The random assembly of immunoglobulin (Ig) genes often creates a B cell receptor that is self-reactive, and such cells are subjected to negative selection. A primary mechanism to extinguish this self-reactivity is receptor editing, which allows continued recombination of Ig genes and replacement of the self-reactive receptor with a new innocuous receptor. Recent data now suggest that receptor editing may also promote autoimmunity in an autoimmune context. This mechanism has also been implicated in the process of B cell positive selection and maturation. Here we discuss the contribution of receptor editing in B-lymphopoiesis and its importance for B cell tolerance and autoimmunity.