Autoantibodies (AABs) have been identified in advanced Covid, laboratory models of Covid-19 utilizing S-protein fragments. The concept that addressing the AABs is a therapeutic target is reasonable, but falls short of addressing the host-targets, the ubiquitous and critical neuroreceptors that have been rendered dysfunctional by these AABs. The a7 nicotinic acetylcholine receptors (a7Rs) rendered dysfunctional are no longer capable of stabilizing the cholinergic anti-inflammatory pathway. In our clinical experience, supported with laboratory collaborations, re-establishing a7R function plays a significant role in both acute COVID-19 as well as Post-Acute Sequelae of Covid. Focusing on therapeutics for Abs 1 or Abs2 appears to be just as short-sighted for PASC as it was for using Monoclonal Abs, IL-6 inhibitors, antivirals for acute COVID-19. The focus should be entirely on the host - targets, the a7Rs and enabling the host's CAP. Ref: doi: 10.1016/biocel.2024.106519