PLXNC1 and neoplasm: These effects were also mediated, at least in part, by Chi3l1 because the ability of Poly(I:C) to inhibit Sema7a and β1 integrin and stimulate Plexin C1 in tumor challenged lungs was significantly ameliorated when Chi3l1 was expressed under the influence of the CC10 promoter (Fig. S1d–f).