KLF6 and Sepsis: M1 polarization can increase KLF6, whereas M2-driving stimuli downregulate its expression.215 KLF6 is required for optimal p65 binding to its M1 target gene promoters, thereby positively regulating the M1 polarization program.216 In contrast, KLF6 interacts with PPARγ to inhibit its induction of M2 gene transcription.216 Lastly, Yuan et al. provide evidence to demonstrate the vital role of KLF14 in regulating the glycolysis of macrophages and sepsis.