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). Here, MET is linked to fibrosis.