KRAS is altered in a minority of gastric cancers, but other components of its network activated by receptor tyrosine kinases are frequently altered, and combining inhibition of the KRAS/BRAF/MEK and the PI3K/AKT cascades with TEAD inhibitors in specific gastric cancer cases with the appropriate target alterations could be a viable strategy. This evidence concerns the gene NTRK1 and gastric cancer.