You just didn't understand that saying, "The point is that evolution included both beneficial and neutral changes. There are lots of mutations and chromosome changes that are synonyms or which have no immediate noticable effect.
Brings the whole reason as to *why* there are so many 'neutral' changes. That is a function of the fault-tolerant *design* of the triplet-codon, diploid, information-coding system.
You mean the *evolution* of fault-tolerance...
Fault tolerance naturally arises through selection in evolutionary processes. See for example:
Evolution of mutational robustnessAbstract: We review recent advances in the understanding of the mutation-selection balance of asexual replicators. For over 30 years, population geneticists thought that an expression derived by Kimura and Maruyama in 1966 fully solved this problem.However, Kimura and Maruyama’s result is only correct in the absence of neutral mutations. The inclusion of neutral mutations leads to a wealth of interesting new effects, and, in particular, to a selective pressure to evolve robustness against mutations.We cover recent literature on the population dynamics of asexual replicators on networks of neutral genotypes, on the outcompetition of fast replicators by slower ones with better mutational support, and on the probability of fixation at high mutation rates.We discuss empirical evidence for the evolution of mutational robustness, and speculate on its relevance for higher organisms.Evolution of Robustness in Digital OrganismsAbstract: We study the evolution of robustness in digital organisms adapting to a high mutation rate. As genomes adjust to the harsh mutational environment, the mean effect of single mutations decreases, up until the point where a sizable fraction (up to 30% in many cases) of the mutations are neutral. We correlate the changes in robustness along the line of descent to changes in directional epistasis, and find that increased robustness is achieved by moving from antagonistic epistasis between mutations towards codes where mutations are, on average, independent. We interpret this recoding as a breakup of linkage between vital sections of the genome, up to the point where instructions are maximally independent of each other. While such a recoding often requires sacrificing some replication speed, it is the best strategy for withstanding high rates of mutation.