This finding is also consistent with the pathophysiological process of sepsis: during severe infections, regardless of whether the primary site of infection is the lung, under the stimulation of inflammatory mediators such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) (25, 26), damage to the pulmonary capillary endothelium is induced, leading to an increase in alveolar-capillary permeability (27), triggering non-cardiogenic pulmonary oedema (28), an increase in respiratory rate, resulting in a decrease in SpO2, an increase in FiO2 and a consequent decrease in the ROX index. The gene discussed is TNF; the disease is infection.