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The second is dose and route translation : even where an effect is real in a mouse, the human-equivalent dose is not a simple body-weight scaling, and as the route section above stressed there is no human bioavailability figure to anchor an oral-versus-injected comparison

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One of these classes (class I ferroptosis-inducing compounds, erastin derivatives) inhibits GPX4 through the depletion of glutathione, and the other (class II ferroptosis-inducing compounds, RSL3 derivatives) inhibits GPX4 directly, without glutathione depletion

Those are either DHA or the EPA