When half a glass of STAT3 is just not enough.

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 dominantnegative effects via forming of nonfunctional STAT3 dimers but some may limit availability of total protein causing STAT3 haploinsufficiency. [ABSTRACT FROM AUTHOR]