NTIS is likely multifactorial, including critical illness-induced HPT axis dysfunction, tissue 5’-deiodinase impairment, and aggregated thyroglobulin, altered thyroid follicular structure, infiltrated monocytes, and depleted thyroid follicles.[36] Currently, there remains controversy regarding the supplementation of thyroid hormone in NTIS patients.[37] In our case, despite severe metabolic stressors (burns, infection, EDKA, CDI), thyroid function normalized without hormone replacement. This evidence concerns the gene TG and infection.