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I'm far from a MASH expert but there was the wonkiness of non-linear results with increasing dosages in the trial and, unless the cause of that can be absolutely nailed down, it can signal untenable uncertainty in future results.

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I proposed that it may be due to imbalances in leronlimab/placebo populations due to CCR5 single or double allele CCR5 delta 32 deletions. They almost certainly looked at CCR5 expression in patients either in the liver environment or in general. They'll be able to look at that patient by patient and see if there was significantly lower or absent CCR5 expression differences between both arms.