Hyper-IgE-syndrome (HIES) is a rare primary immunodeficiency characterized by recurrent skin and pulmonary abscesses, elevated IgE serum levels, and a deteriorating quality of life. Disease-causing mutations in HIES patients are heterozygous and mainly found in the DNA-binding or the SH2-dimerization domain of STAT3. The mutations affecting DNA binding of STAT3 interfere with its function as a transcription factor and impede the activation of downstream target gene expression, such as SOCS3. In this study, we explored the feasibility of correcting the STAT3 gene in patient T cells harbouring the heterozygous mutations K340E or R382W. Both mutations are located in the DNA binding domain, thus preventing downstream target gene activation. We designed a cytosine base editor to correct the K340E allele and an adenine base editor for R382W in order to convert the underlying point mutations back to wild type. Upon optimization of gRNA design and mRNA transfer to patient T cells, up to 98% and 86% of K340E and R382W alleles, respectively, were edited. Based on NGS analysis, our gene editing approach restored wild type STAT3 expression to up to 90% in patient cells. We verified functional rescue of the patient T cells by evaluating STAT3-mediated activation of a downstream target gene. Upon stimulation of base edited T cells with IL-21, STAT3 was phosphorylated and SOCS3 expression upregulated to similar levels as observed in control T cells. In conclusion, our proof-of-principal study demonstrates the feasibility of using base editing in HIES patient T cells to restore physiological expression of functional STAT3.