Formation of Tyk2/JAK2 heterodimer is critical for persistent activation of intratumoral STAT3 and the resistance of targeted therapy, including ESCC cells.24,29 We evaluated whether PCs could stimulate the interaction between Tyk2 and JAK2 in ESCC cells, and found that PC (16:0/20:4) and glycerophosphocholine (10 μM) facilitated the formation of Tyk2/JAK2 complex and the activation of JAK2 in this complex (Supplementary Fig. 13b). This evidence concerns the gene STAT3 and esophageal squamous cell carcinoma.