Finally, the HAdV4-induced pneumonia and CLP-induced sepsis models on wild-type and STING<sup>-/-</sup> mice were used to evaluate the therapeutic efficacy of CSE-P12 and validate its inhibitory mechanisms on the cGAS-STING pathway.<h4>Results</h4>CSE-P12 nanodevices are extensively internalized by macrophages via energy-dependent cellular uptake. The gene discussed is CGAS; the disease is susceptibility to pneumonia measurement.