Lpin1, a downstream target of the PI3K/AKT/mTOR pathway,29 is implicated in lipid synthesis, the sepsis immune response, and ferroptosis.30–32 Ferroptosis, a type of non-apoptotic cell death that is dependent on intracellular iron accumulation, contributes to septic liver injury.33 3-HB affected ferroptosis and the PI3K/AKT/mTOR pathway in various disease models.34,35 However, the mechanisms through which 3-HB inhibits hepatocyte ferroptosis and mitigates liver injury during sepsis via the PI3K/AKT/mTOR pathway remain unknown. The gene discussed is LPIN1; the disease is Sepsis.