Review the KOL talk. On Slide #51 at 38:10 he begins to describe the properties of VB-111. He says: "Main place where you have real angiogenesis is the tumor. We have a lot of things like angiogenesis but they are not real angiogenesis, and this gene is not going to be expressed there." Additionally, the text on that slide suggests that the apoptosis is localized to the tumor microenvironment.
If you want to dive bit deeper, maybe search around for characteristic differences between angiogenesis and neovascularization. TNFa seems to be important enough for him to put on the slide (2nd bullet point) and it does seem to play a role in priming endothelial cells for angiogenesis (https://www.ncbi.nlm.nih.gov/pubmed/18337563). However, TNFa is also implicated in wound healing so I am not convinced that is sufficient to make their drug tumor-specific.
Regarding Avastin being less discriminating, remember that the SeekingAlpha article you mentioned talks about Avastin and it's use in ocular diseases. I found this interesting paper about targeting VEGF/VEGFR to eye diseases (http://www.sciencedirect.com/science/article/pii/S1043661815002856). So it would seem that Avastin acts more broadly.
This is also part of my hunch about why Oren's belief that Avastin leads to poorer quality of life could may be worth following. If you are systemically screwing up angiogenesis and/or neovascularization, I cannot imagine that coming without a lot of pain and soreness. I am very hopeful that this trial succeeds, and then see what they can achieve if they pair VB-111 with a better drug in combination.
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