I've theorized previously that in the CCR5 double allele deletion it would be necessary for a genetic change in other receptors to take up the slack of the missing CCR5. If the other receptors that bound to the same chemokines as CCR5 didn't have wider production and stronger binding then the genetic change of CCR5 double allele deletion would die out. This would happen because of the increased deaths due to a weak immune system.

With other receptors taking the place of CCR5 then of course there would be little difference in the outcome with those with the CCR5 deletion. In those with normal CCR5 expression the inflammatory and autoimmune response is primarily due to CCR5, so leronlimab's blocking curtails those negative responses.