In another in vitro study, S100A8 overexpression in HL-60 leukemia cell line enhanced resistance to etoposide, whereas BCL-2–associated X protein (BAX) and caspase-3 were downregulated at both the mRNA and protein levels, suggesting that S100A8 promotes AML chemotherapy resistance by downregulating the mitochondrial apoptosis pathway [33]. Here, S100A8 is linked to acute myeloid leukemia.