Given that APOE ɛ4 carriers exhibited regional changes in cortical thickness in both directions and a widespread loss of intracortical myelin content compared with non-carriers, one could hypothesize that the contribution of system segregation to the influence of APOE ɛ4 on PI might be attributed to the impact of GM atrophy on FC and/or system segregation. The gene discussed is APOE; the disease is Atrophy.