Since VEGF and bFGF produced by primary tumor cells also contribute to promoting cell proliferation in an autocrine manner (Cao et al., 2012[3]; Berger et al., 1999[2]), the inhibition of pro-angiogenic factor secretion by MLE (Figure 4(Fig. 4)) may partially explain the growth-inhibitory activities of MLE (Figure 1(Fig. 1)). The gene discussed is FGF2; the disease is neoplasm.