STAT3 and severe congenital neutropenia: These findings are consistent with recently published data from Link's group in which expression of a truncated mutant murine G-CSFR form (d715F) in mice that is equivalent to the Δ716 human G-CSFR in patients with SCN/AML was found to confer a strong clonal advantage that was dependent on Stat5, but not Stat3 [35].