However, we were surprised to find that overexpression of GPR162 significantly down-regulated the expression level of cGAS protein in liver cancer and lung cancer cells, whereas the cGAS inhibitor (Ru.521) did not affect the transcription level of signaling molecules downstream of STING, while the STING inhibitor (C-176) could significantly inhibit the transcription of downstream molecules (Fig. 2m–p, Supplementary Fig. 3h–q). Here, GPR162 is linked to lung carcinoma.