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It only performed good in those with many more CCR5 surface receptors expressed than normal.

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and in the 700 mg group with genetic haplotypes known to over produce CCR5 compared to placebo

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"compared to placebo" not compared to normal. We'd have to know what haplotype types differed between the three groups to make a proper assessment.

When you say it performed good in only those with more CCR5 receptors you would be wrong. Mean percent change from baseline PDFF - 700 mg group (+3.75% vs +9.85%, p = 0.135). Mean change cT1 - 700 mg group (-2.73 ms vs +27.64 ms, p = 0.059). Those numbers would switch to statistically significant with a larger patient population.

The 700mg haplotype did better than the 700mg group over all. But the outcomes are based on a difference between baseline and end of trial. One would assuredly see a greater difference with a CCR5 blocker if there's more CCR5.

But why would 350mg be higher than not only the entire 700mg group but also the 700mg haplotype group? In the paper baseline levels of cT1 and PDFF in 700mg were not broken out like they were for 350mg. Which could be because of very similar baselines in 700mg that were lower than for 350mg. Remember the p value is based on the difference between baseline and end of trial. With lower disease severity you would of course have a smaller difference and that could be why 350mg beat 700mg. It would also explain the vast difference in chemistry and serum markers between 350mg and 700mg.