STING1 and renal cell carcinoma: To find approaches to disrupt STING binding with VDAC2 in treating RCC, we found palmitoylation of STING‐C88/C91 residues played a critical role in mediating STING binding to VDAC2 and genetic depletion or pharmacological inhibition of ZDHHC palmitoyltransferases efficiently disrupted the STING‐VDAC2 interaction leading to inhibition of cell growth in RCC.