In sepsis models, poly (lactide-co-glycolic acid)-encapsulated FMN (PLGA-FMN) significantly upregulates PRDM16 expression and activates the NRF2/GPX4 pathway, effectively inhibiting ferroptosis and reducing sepsis-associated multiorgan injury, including lung damage (Zheng et al., 2024). The gene discussed is PRDM16; the disease is Sepsis.