As a result, excessive inflammatory cytokines grow up into the local cytokine storm and induce acute lung injury.143 Furthermore, lung injury sustains the cascade amplification of inflammatory effect and leads to systemic inflammation.144 Moreover, IFN-γ activates aryl hydrocarbon receptor (AhR) on AT II cells, leading to upregulation of the expression of ACE2 and mucins.145,146 Consequently, the infection expands, and redundant mucins deposit and gradually impair the exchange of O2 and CO2. Here, ACE2 is linked to infection.