In the process of antibody affinity maturation, somatic hypermutations (SHMs) are introduced into the variable region of B cells activated by a specific antigen, and clones with increased affinity to the target antigen are selected from among the mutant antibodies generated. Our research goal is to elucidate the mechanism of generation of high-affinity antibody-producing B cells, called antibody affinity maturation, and the mechanism of SHM, which is estimated to be one million times more frequent than spontaneous mutations. In addition, dysregulation of SHM is thought to be associated with diseases that occur as a result of genomic instability. We have discovered that a splicing variant SRSF1-3 of serine-arginine-rich splicing factor 1 (SRSF1) is involved in SHM. We are investigating the regulatory mechanism of SHM by analyzing the structure and function of SRSF1-3.