On 2017 Oct 12, Sander Houten commented:

This paper focuses on the role of KLF14 in insulin signaling via the PI3K/Akt pathway. The authors study mouse models of obesity and the Hepa 1-6 cell line, a derivative of a mouse hepatoma. The authors show that Klf14 mRNA and KLF14 protein expression is decreased in liver, adipose and muscle of C57BL/6 mice on high fat diet and db/db mice when compared to control animals. In subsequent experiments the authors use ectopic KLF14 expression in Hepa1-6 cells and show that KLF14 stimulates insulin signaling via the classical PI3K/Akt pathway (Yang M, 2015). I would like to point out that there is little evidence to support the hypothesis that KLF14 plays an important role in adult mouse liver biology. We found no evidence for expression of KLF14 in adult mouse liver as we were unable to amplify Klf14 cDNA, did not find Klf14 mapped reads in liver RNA sequencing data and found no specific signal upon immunoblotting (Argmann CA, 2017). Our data on the absence of Klf14 expression in liver are consistent with previously published work by others (Parker-Katiraee L, 2007) and publicly available data sources. We also investigated the physiological functions of KLF14 by studying a whole body KO mouse model and focused on the metabolic role of this transcription factor in mice on chow and high fat diet. Our results indicate that KLF14 does not play a role in the development of diet-induced insulin resistance in male C57BL/6 mice (Argmann CA, 2017).

On 2017 Oct 12, Sander Houten commented:

This paper focuses on the role of KLF14 in insulin signaling via the PI3K/Akt pathway. The authors study mouse models of obesity and the Hepa 1-6 cell line, a derivative of a mouse hepatoma. The authors show that Klf14 mRNA and KLF14 protein expression is decreased in liver, adipose and muscle of C57BL/6 mice on high fat diet and db/db mice when compared to control animals. In subsequent experiments the authors use ectopic KLF14 expression in Hepa1-6 cells and show that KLF14 stimulates insulin signaling via the classical PI3K/Akt pathway (Yang M, 2015). I would like to point out that there is little evidence to support the hypothesis that KLF14 plays an important role in adult mouse liver biology. We found no evidence for expression of KLF14 in adult mouse liver as we were unable to amplify Klf14 cDNA, did not find Klf14 mapped reads in liver RNA sequencing data and found no specific signal upon immunoblotting (Argmann CA, 2017). Our data on the absence of Klf14 expression in liver are consistent with previously published work by others (Parker-Katiraee L, 2007) and publicly available data sources. We also investigated the physiological functions of KLF14 by studying a whole body KO mouse model and focused on the metabolic role of this transcription factor in mice on chow and high fat diet. Our results indicate that KLF14 does not play a role in the development of diet-induced insulin resistance in male C57BL/6 mice (Argmann CA, 2017).