HGF/c-Met signaling, for example, prevents TGF-β1-induced EndoMT in cardiac fibrosis (Okayama et al., 2012; Wang et al., 2018) but c-Met signaling activates EndoMT and abnormal vessel growth in glioblastoma (Huang et al., 2016) potentially compensating for the loss of VEGFR2 in these tumor vessels described by Liu et al. (2018). This evidence concerns the gene TGFB1 and neoplasm.