MYD88 and asthma: 2018). The knockdown of HMGB1 reduces the severity of asthma by reducing airway smooth muscle thickness, collagen deposition, mucus secretion, and inflammation in the airway (Hou et al. 2015). The TLR-4 protein, the receptor for HMGB1, is involved in the immune cell response and in inflammation, and its overexpression in the lung enhances the thickness of the airway wall by activating elastase and NF-κB (Wang et al. 2020). The MyD88-dependent pathway is used by TLR-4 to activate NF-κB and further contributes to the synthesis of inflammatory cytokines (Liu et al. 2017).