For example, upregulation of Bmal1 in LPS-treated H9C2 cells increased cell viability by reducing ferroptosis and the accumulation of reactive oxygen species and lipid hyperoxides (28), whereas Bmal1 depletion increased mortality in C57BL/6J male and female murine models of sepsis following caecal ligation and puncture (CLP) (29). This evidence concerns the gene BMAL1 and Sepsis.