My primary research focuses on the pathogenesis of autoimmune diseases and allergy in the perspective of pre-mRNA alternative splicing. Alternative splicing of pre-mRNA increases protein diversity and expands proteome with certain number of genes. Protein isoforms of different cellular functions may be generated by alternative splicing. Recent technologies revealed that more than 95% of multi-exon genes in humans undergo alternative splicing, including FOXP3 that is a transcription factor for the development and function of regulatory CD4 T cells. Human FOXP3 gene is expressed as two major isoforms: the full-length isoform and the short isoform. The short isoform does not contain the region coded by exon 2. My previous work identified the functional difference between the two FOXP3 isoforms in the suppression of genes that define Th17 lineage. My current studies, using a Foxp3 exon2-deletion mouse strain, have shown the essential role of exon 2 for FOXP3 to maintain the immune tolerance.