When half a glass of STAT3 is just not enough

Abstract

In this issue of Blood, Bocchini et al report a novel mechanism by which STAT3 mutations result in an unstable protein and give rise to a reduction in STAT3 signaling, suggesting that pathogenic mutations do not always confer dominant-negative effects via forming of nonfunctional STAT3 dimers but some may limit availability of total protein causing STAT3 haploinsufficiency.1