Function and another failure to consider the null hypothesis

Somehow, the following kind of illogic creeps into so many discussion of genomic function:

In terms of pathological functions, somatic mosaicism of terminally differentiated cells has long been known to cause cancer. Recent work shows that somatic mosaicism of nervous system tissues underlies a host of neurodevelopmental and perhaps neuropsychiatric diseases (17). However, the extent of somatic mosaicism that is now being reported in a variety of healthy tissues and cell types suggests that it also has physiological functions.

– James R Lupski, “Genome Mosaicism—One Human, Multiple Genomes” Science 26 July 2013: Vol. 341 no. 6144 pp. 358-359

This paragraph comes after the author carefully describes why extensive mosaicism is unavoidable, given the number of cell divisions we undergo during development from a zygote into a fully adult human.

So explain to me why extensive mosaicism “suggests that it also has physiological functions”? Why should we think that most of the mosaicism being observed is anything like the deliberate hypermutation that happens in the immune system? Isn’t the default hypothesis that mosaicism is the expected, non-functional by-product of trillions of cell divisions?

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