Chunk #29 — From large-effect risk loci to disease biology — The CHRNA5–CHRNA3–CHRNB4 nicotinic receptor gene cluster and the CYP2A6 nicotine-metabolising gene.
These biological mechanisms are inherently pharmacogenomic [G] effects. SUD genetics is, in a very real sense, a pharmacogenomic application: it reflects the interaction of the body with exogenous substances. The principles are essentially the same as when dealing with a therapeutic endogenous substances; indeed, some abusable substances, like opioids used for pain, are themselves sometimes therapeutic, depending on context.
