Since STING‐C91A/C88A mutant is deficient in binding VDAC2 (Figure 3Q), and STING palmitoylation on both C91 and C88 were observed to maintain STING function on Golgi,[46] we reasoned that inhibiting STING palmitoyltransferase(s) would be an approach to maximize tumor inhibition. Here, VDAC2 is linked to neoplasm.