What the work claims
Most molecular evolutionary change and genetic variation within and between species arise from random drift of neutral mutations—not natural selection. Most non-deleterious mutations are neutral, not beneficial. Neutral alleles fix by chance sampling, not selective advantage.
How it was done
Kimura introduced the theory in 1968 using Haldane’s estimate of fixation time for beneficial mutations to show the human–chimpanzee substitution rate exceeded what selection alone could explain. He developed the infinite sites model and combined theoretical population genetics with molecular evolution data.
What holds up
The prediction that substitution rates equal per-individual mutation rates—and are independent of population size—holds where neutrality applies. The inverse correlation between functional constraint and divergence rate is empirically robust. Within-species variation scaling with effective population size is widely observed.
What does not
The theory does not prove most mutations are neutral. It does not refute selection at the phenotypic level. It does not resolve whether a given polymorphism is neutral or selected—it only provides null expectations against which selection can be tested.
Why it matters beyond the lab
It underpins modern molecular phylogenetics, genome-wide scans for selection, and interpretations of human genetic diversity. It forced evolutionary biology to distinguish process (drift vs. selection) from pattern (sequence change), making molecular data interpretable.
Is it worth your time
Yes. It redefined how we interpret molecular variation—shifting focus from adaptation to drift—and remains foundational for calibrating molecular clocks, detecting selection, and analysing genomic data.