S100A8 and cystic fibrosis: In contrast to pro-fibrotic actions of HMGB1, S100A8, and S100A9 due to expression induction of ECM components such as collagens, promotion of myofibroblast transition including SMA generation, and finally CF proliferation (Zhang et al, 2012), S100A1 exerts a time- and dose-dependent anti-fibrotic profile.