To determine the clinical significance of these findings, we queried transcriptomes of human keloids compared to matched non-lesional skin46 and of mechanically stressed mouse wounds that progress to hypertrophic scars47, and found that many of the activin-regulated matrix genes were among the top up-regulated genes in these datasets, including Postn, Plod2, Wisp1, and Lox, with Col3a1, Aspn, and Cthrc1 being also in the annotated disease-gene association network for keloids48 (Fig. 3i). The gene discussed is INHBE; the disease is keloid.