Suggesting the synergistic action of LC3 and Bcl-xL on HS pathogenesis, and moreover, silencing for Bcl-xL was found to increase the apoptosis of HSFs (Figure 5), and reduce the formation of HS after wound closing in a rabbit ear scar model (Figure 6 and 7). The gene discussed is MAP1LC3A; the disease is histiocytic sarcoma.