The ability to selectively target VEGFR2 also supports the rationale for combination approaches based on drug mechanism of action; for example, VEGF signaling has been shown to suppress T cell priming and induce T cell exhaustion, providing rationale for anti-VEGFR plus immune checkpoint blockade combinations, as both classes of drugs may result in increasing the anti-cancer T cell efficacy [27]. Here, VEGFA is linked to cancer.