CALCR and Fabry disease: The thematic analysis showed that (I) telomere length, especially in early disease stages, (II) BDP methylation by sphingolipids, (III) epigenetic reader proteins, (III) mtDNA haplogroups H and I and cluster HV, and (IV) DNA methylation of the promoter region of the calcitonin receptor gene in individuals on ERT could potentially function as molecular mediators of clinical variability in Fabry disease and is summarised in Figure 3.