While the proper formation of the HF structures is particularly impaired by Rac1 excision, the delay in skin wound healing may result from the direct effects of Rac1 on the IF stem cell population or on the ability of their derived transit amplifying cells to proliferate, migrate and terminally differentiate to repopulate the wound area quickly, thereby reestablishing the epithelial barrier function. This evidence concerns the gene RAC1 and hydrops fetalis.