Hypotheses

1.  With each succeeding generation, we'd see a greater and greater percentage of the population with significant physical and/or cognitive limitations affecting quality of life due to defects in multiple genes.

• I have a significant disability (unable to do job requiring physical labor, standing all day, and working with my hands day in and day out).  More than one gene involved which uric acid transport is dysfunctional (ABCG2 and SLC2A9).
• Succeeding generations have more mutations than their parents due to copy errors.
• The defect in each gene is not "seen by" natural selection even though there is some loss of function associated with the mutation.
• Over time, more people will have loss of function defects in multiple genes involved in similar functions.  Which could lead to physical and/or cognitive limitations but not necessarily overt genetic disease.

2.  The severity of erythropoeitic protoporphyria (EPP) corresponds to the level of ABCG2 function in addition to the type of FECH mutations. 
3.  Genes located near each other have some type of overlapping function.  Genes of uncertain function may have something in common with nearby genes.