To explore whether RGS could directly induce CD40 expression in melanoma cells, and if so, which RAS-mediated pathway(s) may be responsible for the phenotype, we evaluated the impact of serval pathway specific inhibitors on CD40 plasma membrane expression in melanoma cells in vitro, including mTOR kinase inhibitor PP242 (5 μM), mTORC1 inhibitor Everolimus (10 nM), MEK inhibitor Trametinib (0.1 μM), BRAF inhibitor Dabrafenib (1 μM), AKT inhibitor Ipatasertib (10 μM), and/or RGS (0.1 μM). Here, AKT1 is linked to melanoma.