In fact, although no direct reports were seen on the extent of the contribution of renal tissue-resident Gli1+ MSC to the myofibroblast pool after renal IRI, it has been shown that Gli1+ MSC-like cells, which account for less than 0.2% of the total PDGFRβ+ renal cell population, are reported to be the source of approximately 50% of myofibroblasts in a murine model of unilateral ureteral obstruction kidney injury and are considered to be the most predominant cell population involved in renal fibrosis [27]. Here, GLI1 is linked to renal fibrosis.