To functionally explore the mechanisms by which miRNAs contribute to T2D pathogenesis, two miRNAs (miR-548 and miR-607) were selected for follow-up experiments in primary human muscle cells based on (i) being upregulated in muscle from twins with T2D versus co-twins without T2D (Fig. 4E and Additional file 1: Supplemental Table 12) and (ii) having significantly more predicted targets than expected by chance for genes found to be dysregulated in the “GLUT4 translocation” and “signaling by receptor tyrosine kinases” pathways, respectively (Table 2 and Additional file 1: Supplemental Table 2). This evidence concerns the gene NTRK1 and type 2 diabetes mellitus.