Interestingly, some of the loss of function mutations observed in tumors are reported to affect the receptor kinase domain (e.g., the missense R411Q [41], and the truncating W406*, S462*, and E470* mutations [42–44]) and have already been described in human hereditary telangiectasia (HHT)2, an autosomal dominant genetic vascular disorder caused by mutations in ACVRL1. Again, these events were randomly distributed in the different datasets and did not confer any overt advantage to the tumors. Here, ACVRL1 is linked to telangiectasia, hereditary hemorrhagic, type 2.