TLR4 and tuberculosis: Only miR-23a-3p and miR-155-5p were consistently down-regulated both in active TB patients and in response to Mtb-specific antigen stimuli in vitro, while miR-155 has been demonstrated to be able to eliminate mycobacterial infection through augmenting apoptosis, autophagy, and ROS production via targeting Rheb/SHIP1/TLR4 signaling in previous studies [13,14,15,16,17,18].