In regard to the finding that UA and/or mTOR inhibition differentially modulated UVR-induced NF-κB activation and mitochondrial oxidative stress in skin melanoma versus RPE cells, we speculated that NF-κB activation of RPE cells is decreased through UA-mediated insulin/IGF-1-dependent anabolic metabolism against mTOR activity, while the hyperactive tyrosine kinase of IGF-1 receptor in skin melanoma cells manifests NF-κB activation and mitochondrial oxidation via the PI3K-AKT cascade (Figure 3) [18]. Here, AKT1 is linked to cutaneous melanoma.