As mentioned above, RNA editing is correlated with the emergence of resistance[31]; organoid lines from resistant patients with the intestinal subtype of gastric cancer (GC) showed upregulation of JAK/Src-signal transducer and activator of the transcription (STAT) signaling and adenosine deaminases acting on RNA 1 (ADAR1), along with hyper-edited lipid metabolism genes due to A-to-I editing on the 3’UTR of stearoyl- CoA desaturase (SCD1). The gene discussed is SOAT1; the disease is gastric cancer.