In contrast to novel drugs, which target the general ubiquitin proteasomal machinery by inhibiting their core components, such as Nedd8-activating enzymes, the SCF-adaptor Skp1 or the proteasome, and thus providing therapeutic chances for cancer, neurodegenerative diseases and immune deficiencies, a drug against Fbx15 would not affect the ubiquitin-proteasome system itself, but instead offer a highly specific inhibitor for fungal dissemination during life threatening aspergillosis [5,26,68,69]. This evidence concerns the gene KITLG and Immunodeficiency.