There have been two studies reporting the regulatory role of PU.1 on S100A9 expression at the transcriptional level in chronic inflammation processes during aging and progression of promyelocytic leukemia [28, 29], but our data showed that PU.1 not only transcriptionally promoted expression of S100A9 but also S100A8 in humans and mice. Here, SPI1 is linked to acute promyelocytic leukemia.