Stromal cells constitute large portions of GC tumors, and cancer‐stromal cell interactions promote tumor growth and metastasis.38 Coexistence of often benign gastro‐stromal intestinal tumors (GISTs) with gastric adenocarcinoma has been frequently observed.23 In our TCGA‐GCC analysis, a KRAS dependent GC tumorigenic module (M28) associates to varying degree of “stromal‐ness.” This stromal‐ness corresponded to GIST specific oncogenic mutations, KIT and PDGFRA,23 pertaining stromal–epithelial interactions in GC. This evidence concerns the gene KIT and gastric adenocarcinoma.