Such hypothesis is in line with recent findings by other groups: Ding et al. [23] reported that Rcn3 showed a high expression in immune cells and fibroblast cells in Pan-cancer analysis; Park et al. [24] showed that Rcn3 was a pivotal regulator of collagen fibrillogenic during postnatal tendon development; Liu et al. [25] observed that Rcn3 was significantly up-regulated in keloids, in which abundant fibroblasts and collagen deposits involved. The gene discussed is RCN3; the disease is keloid.