Regardless of EBV status, most gastric cancers have at least one aberrancy in a druggable pathway such as receptor tyrosine kinase signaling.10, 73, 74, 75, 76, 77, 78, 79 Newly identified in ‘genomically stable' gastric cancers is activated RHOA singaling via mutation of RHOA GTPase, or fusion events in RHOA inhibitors (ARHGAPs), broadening the opportunity to test inhibitors of the RHOA effector ROCK that are well studied in vascular biology. Here, NTRK1 is linked to gastric cancer.