Another study showed that the inhibitory effects of the ApoA-I mimetic peptide D4-F was dependent on the upregulation of the antioxidant enzyme manganese superoxide dismutase (MnSOD), as silencing of the gene in the engrafted cells by a MnSOD-specific shRNA abolished the D4-F-tumor suppressing effects, suggesting that the antioxidant activity downstream of ApoA-I may be essential for its tumor suppressor properties in OC [153]. Here, APOA1 is linked to neoplasm.