In this regard, the first hypotheses derived from the observation of basophilia in an experimental murine model developing SLE-like disease (including nephritis), namely the Lyn−/− (which is a Src family protein tyrosine kinase) knock-out murine model; indeed, it exhibits a constitutive Th2-shifted immune response leading to an IgE- and IL-4-dependent nephritis, with glomerular deposition of circulating immune complexes (CICs). This evidence concerns the gene SRC and nephritis.