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). This evidence concerns the gene SEMA7A and neoplasm.