While this study has preliminarily revealed the concentration-dependent mechanism by which HO-1 regulates cognitive function through the Exos-mediated lung–brain axis, several aspects require further refinement: First, although the experimental hypothesis links the neurotoxic effects of HO-1 to ferroptosis, the absence of intervention experiments using ferroptosis-specific inhibitors prevents direct confirmation that HO-1-induced ferroptosis represents the core pathway underlying HO-1-mediated cognitive impairment. The gene discussed is HMOX1; the disease is Cognitive impairment.