In our study, GO analysis showed that targets of DE miRNAs in lipedema tissue were enriched in intracellular steroid hormone receptor signaling pathway changes, whereas KEGG pathways highlighted endocrine resistance, including insulin and prolactin signaling pathways to act through loss or modification of estrogen receptor activity; it has been hypothesized that impaired estrogen receptor expression and signaling may be involved in the onset of lipedema, as estrogen affects lipid metabolism directly, especially in white adipose tissue via its receptor [39]. This evidence concerns the gene INS and Lipedema.