Even if the clinical diagnosis and inclusion criteria for CLPD-NK36 patients in the two cohorts were homogeneous, a lower proportion (14% vs. 60% from Jerez et al.7) of symptomatic patients in our cohort can possibly explain the molecular differences that have been observed, considering that a relation between the development of symptoms (mostly related to neutropenia) and the presence of STAT3 mutations has been reported16. This evidence concerns the gene STAT3 and Decreased total neutrophil count.