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. Here, VDAC2 is linked to renal cell carcinoma.