Epigenetically, global hypomethylation in GD coexists with locus- and pathway-specific changes, including hypermethylation/reduced active histone marks at TSHR and distinct DMP/DMR signatures separating GD from HT—even persisting after treatment, which argues that epigenetic state is not merely a consequence of thyroid status [16,20,21,22,52]. Here, TSHR is linked to hematocrit.