Ets-1 belongs to the ets family, which consists of transcription factors involved in vasculo- and angiogenesis. Although we found downregulated Ets-1, Ets-1 null mice are viable, probably due to redundancy among ETS members. Therefore, the mechanism that explain embryonic lethality in the absence of PRKCD and PRKCE cannot be explained through a pathway that only involves ETS-1. We thus looked further within the same family in an attempt to find a candidate whose deficiency could be consistent with the phenotype displayed by Prkcd and Prkce double SKF38393 HCl deficient embryos, and were able to identify downregulated Fli-1, an ets family member whose deficiency in mice leads to embryonic lethality due to hemorrhage and disrupted vessel integrity at approximately E12.5. However, conditional deletion of Fli-1 in the endothelium does not prevent mouse viability, although it regulates genes involved in vascular homeostasis, such as Cdh5 and Cd31, which are downregulated in Prkcd and Prkce double deficient embryos. This therefore opens the possibility to the existence of a mechanism involved, at least, in vascular homeostasis where Prkcd and Prkce might regulate Cdh5 and Cd31 via Fli-1 and Ets-1, since these genes are all regulated in Prkcd and Prkce double deficient embryos. We also looked into mRNA levels via semiquantitative PCR for Mef2c, a transcription factor that contains essential ETS binding sites for vascular development and viability in mouse embryos at E9.5, but did not observe any clear regulation in double deficient embryos, which could be due to redundant function that exists within the Ets family. The observed significant downregulation of the endothelial markers Cd31 and Vegfr2 in double deficient embryos via qPCR could also be due to fewer endothelial cells present in double deficient embryos. Indeed, Flk-1 deficient mice die at E8.5 and display impaired vasculogenesis, so Flk1 seems to lie upstream Prkcd and Prkce. Cd31 deficient mice, however, are viable and do not display a vascular phenotype, so PRKCD and PRKCE TAS-102 dependent Cd31 expression should not be crucial in mouse viability.