Thus, we hypothesize LPS-induced miR-34a targets Klf4, which is a proven target of miR-34a [36], promotes pro-inflammatory M1 phenotype, and worsens acute lung injury (ALI) in coordination with MAPK/ERK; therefore, inhibition of miR-34a would be beneficial in terms of ALI and macrophage polarization status. Here, KLF4 is linked to acute respiratory distress syndrome.