In the mouse model of Rett syndrome the changes are nutrient-dependent. This links the epigenetic effects of choline to intercellular signaling, amino acid substitutions, and stochastic expression of newly created genes in the mouse-to-human model of nutrient-dependent pheromone-controlled amino acid substitutions, de novo creation of genes and chromosomal rearrangements.
I used the mouse-to-human model as an example with other examples of ecological adaptations that refute the theory of mutation-driven evolution. My model shows that mutation-initiated natural selection is not biologically plausible or ecologically valid because mutations perturb the protein folding required for increased organismal complexity.
“Dobzhansky  and Muller , partially preceded by Bateson [3,7,10] proposed that hybrid sterility and inviability are caused by incompatible alleles alternatively fixed in two previously isolated populations (BDM model). The BDM model is so straightforward that it became the null model of speciation  and except for a few strong proponents (notably [1,2]) chromosomal speciation was largely neglected.”
With no experimental evidence whatsoever, a proposal became accepted as a model of speciation because the model was straightforward. Biological Laws were excluded. Darwin’s ‘conditions of life’ were excluded. The physiology of reproduction was excluded. Ecological factors were excluded.
I realize why it’s been so difficult for people to understand my model. It includes too many things that were excluded in the null model of speciation, which they accepted because it was so straightforward.
If I eliminated biologically-based cause and effect from my model, it would be equally straightforward.
It would not be a model of ecological adaptations. It would be nonsense akin to the straightforward null model of speciation (i.e., mutation-driven evolution).