Thanks so much gestalt2 for that. The picture sho

Thanks so much gestalt2 for that. The picture shown here:

https://www.nature.com/articles/s41577-021-00639-3/figures/1

really made me understand that in early phases of NAFLD, the immune system was not even being activated or recruited. It is in the later phases of NAFLD and then NASH when the immune system is recruited and activated.

It is only then when LL may have any effect at all.
Possibly, in the 700 HM group, with many more CCR5 surface receptors on the hepatocytes, their binding to LL may help the hepatocyte reduce the steatosis that occurs in early phases of NAFLD with a NAS of 1 or 2. Where as, with normal or low surface expression of CCR5, the binding of LL to CCR5 was insufficient to cause any change within the hepatocyte b/c there wasn't sufficient quantities of CCR5 on the hepatocytes surfaces to effect any change in steatosis, but with 700 HM group, there were many more CCR5 surface receptors which were all bound by LL which effected improved cT1 and improved PDFF in the 700 HM group.

If the 700 treated group were relatively healthy, of NAS 3 or less and were treated with 700mg LL, it would be like they were receiving Placebo which is what the heat map looks like. Just compare the vertical column of the Placebo to the vertical column of 700mg and they look identical. Why? because the 700mg patients had to be quite healthy to start with. If you don't have the immune system being recruited and activated, then there is nothing for LL to bind to. Since in this group, you only have normal CCR5 surface receptor quantity expressed on the hepatocytes, there is insufficient CCR5 quantity to effect any changes in steatosis. The 700 HM group showed that with increased CCR5 receptor expression, when bound to LL, the PDFF was significantly reduced.

Thank you so much for appreciating my answer.