This is probably due to the increased accessibility of Tyr291 residue of WASP to the tyrosine kinase, consistent with the previous finding, which showed that the activating mutation of WASPL270P (identified in patients with severe congenital neutropenia) stabilizes WASP in an open conformation37, and increases Tyr291 phosphorylation of WASP27, 38. This evidence concerns the gene WAS and severe congenital neutropenia.