We focused on BC proliferation as the primary phenotype and, based on our observation that levels of the fast-migrating SPRY2 isoform were decreased in the Fgfr1 cKO cells (Figures 3B and 3C), we hypothesized that a major role of FGFR1 signaling in the tracheal BCs is to modulate SPRY2 activity and, moreover, that the function of SPRY2 in these cells is to inhibit signaling activity downstream of RTKs other than FGFR1, for example EGFR, which is necessary for tracheal BC proliferation (Brechbuhl et al., 2014, Lu et al., 2013). Here, SPRY2 is linked to breast cancer.