For example, Cbl-null mice show increased cellularity in the hematopoietic organs [13-15] whereas Cblb-null mice exhibit hyper-responsiveness to immunological insults leading to autoimmunity [16, 17]; this phenotype was further augmented to a fulminant inflammatory disease when Cbl and Cbl-b were concurrently deleted in the T cell compartment [18]. The gene discussed is CBLB; the disease is Autoimmunity.