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I don't think it is a good idea to cast doubt on the validity of the biomarker data. I'm sure CR looked into this over the past 6 months when the data was so unusual.

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When the biomarker results directly contradict the actual results then there should be doubts. In 700mg it does.

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We saw reductions in cT1 with 700 mg HM only. Not in 700 normal.

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wrong

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Mean change cT1 - 700 mg group (-2.73 ms vs +27.64 ms, p = 0.059).

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700 mg normal was worse than placebo because it increases CD8 natural killer cells like CR says

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The switch to an M1 macrophage phenotype correlates with an increase of CD8 NKT cells. Furthermore that M1 phenotype also shows a decrease in inflammatory biomarkers. As I've said before the quantitative effect between 350mg and 700mg is simply a matter of receptor occupancy.

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It is very clear what happens when you have huge numbers of CCR5 and 700mg HM because that was demonstrated to work well. Why was the data acceptable to you in the HM group and not in the normal 700 group?

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I will repeat what I previously posted. The biomarker data is shown as the difference between baseline and trial end. With a higher level of CCR5 in the haplotype variant you will of course see a greater difference even if the testing was bad.

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In fact, the body scars and produces scar tissue in an effort to contain the dying hepatocytes. The hepatocytes are inflamed and being attacked by the immune system because they are dying. So, the HSCs or Hepatic stellate cells begin to induce scarring which is an effort to reduce and contain the inflammation.

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Initially it's the over-inflammation that causes those cells to die off.. The immune response increases above it's already high level due to that cell death. That increased inflammatory response leads to increased collagen deposition leading to the scarring. Leronlimab reduces collagen and the inflammation.