Jensen et al. generated a conditional transgenic mouse that expressed the alternative splicing factor serine/arginine-rich splicing factor 6 (SRSF6) in the skin. They found that SRSF6 induction caused substantial hyperplasia and skin thickening, which was enhanced by epidermal injury. SRSF6 induction also caused the activation of genes that are involved in wound healing. The authors found that SRSF6 is overexpressed in several types of skin cancer. Together, these data indicate that SRSF6 is a proto-oncogene that drives wound healing and hyperplasia.