CSF3R and severe congenital neutropenia: To further investigate the role of ubiquitination in G-CSFR-mediated cell proliferation, we generated a mutant form of the G-CSFR (K762R/G-CSFR) which abrogates the attachment of ubiquitin molecules to the lysine residue at position 762 of the receptor that is deleted by mutations in the G-CSFR in patients with SCN/AML.