Abnormalities in both receptor oligomerization and trafficking have been shown to alter normal receptor function and ligand sensitivity and to contribute to human diseases [13]–[16].Our laboratory previously reported that ligand internalization and receptor degradation are impaired leading to sustained cellular activation and enhanced cell survival and proliferation in patients with severe congenital neutropenia (SCN) transforming to (AML) in which a truncated G-CSFR is expressed along with the wild type form [17]. The gene discussed is CSF3R; the disease is severe congenital neutropenia.