This disease is characterized by an excessive production of heavy chains that are short and truncated. These heavy chain disease proteins have various deletions, mainly in their amino-terminal part, which causes the heavy chains to lose the ability to form disulfide bonds with the light chains. The defect in the immunoglobulins presumably arises during somatic hypermutation.[2] Deletion of the N-terminal part of the heavy chain disease protein leads to aggregation and signaling of the B cell receptor,[3] presumably due to the loss of the anti-aggregating properties of the light chain.[4]