In contrast, dermal fibroblasts are positive for expression of both S100a4 and α-SMA (Österreicher et al., 2011) and Chen et al. (2015) demonstrate that S100a4 treatment increases α-SMA expression, while α-SMA+ cells decrease with S100a4-cell depletion in a model of liver fibrosis. Using a similar combination of S100a4-lineage tracing and active S100a4 expression analyses as in Österreicher et al. (2011), we demonstrate that S100a4Lin+ cells become α-SMA+, and that the α-SMA+ population is largely negative for S100a4. Here, ACTA1 is linked to Hepatic fibrosis.