Pharmacogenomics can identify inherited differences in drug metabolism, transport, targets, and toxicity risk, but genotype is a stable biological descriptor rather than a complete representation of the patient’s current pharmacological state. A DNA result does not directly observe phenoconversion, inflammatory suppression of drug-metabolizing pathways, organ dysfunction, interacting medicines, medication-taking behavior, or the exposure actually achieved during therapy. This Perspective argues that precision dosing should preserve validated genotype information while repeatedly reconciling it with dynamic phenotype and exposure information. Evidence from pharmacogenomic guidelines, genotype–phenotype concordance studies, phenoconversion research, inflammatory pharmacology, drug–drug–gene interaction modeling, adherence science, and therapeutic drug monitoring supports the component distinctions, but not a universal integrated dosing algorithm. We therefore treat genotype as a durable prior, dynamic phenotype as a state-dependent modifier, and measured exposure as feedback that can confirm or challenge earlier expectations. The resulting approach is intentionally conditional: the value and weighting of each information layer depend on the drug, pathway, therapeutic index, treatment phase, assay, population, and clinical question. Precision dosing is consequently better framed as longitudinal evidence reconciliation than as a one-time translation from DNA to dose.
IJPRAS
