The rise in COHb% shown in non-survivors around day 6 in our study could be explained by these cytokines, an oxidative stress-mediated pro-inflammatory state, high HO-1 expression, and these factors combined. Additionally, non-survivors in the second week of illness displayed a decrease in oxygenation and impaired respiratory ability to eliminate COHb due to the development of ARDS, underlying sepsis [18-20], and hemolysis (drug and viral-illness mediated). The gene discussed is HMOX1; the disease is Sepsis.