To determine whether there were changes in DDR2 signaling in this panel of tumor cell lines, we utilized a commercially available phosphorylation array to measure phosphorylation of downstream signaling mediators in response to collagen I. In both parental BT549 cells and WT-rescued cells there was increased phosphorylation of FGR, HSP27 (also known as HSPB1), JNK (JNK1–JNK3, also known as MAPK8–MAPK10), p38α (also known as MAPK14), PDGFR-β, PLC-γ (also known as PLCG1) and STAT2 when compared to that in DDR2-depleted cells (Fig. S1C). This evidence concerns the gene STAT2 and neoplasm.