Clinical trials with the inhibitors of PI3K/AKT/mTOR pathways may be favourable for melanoma patients with specific mTOR mutations.31 In the present work, it was found that IGF‐1 improved the UM cell viability and activated the IGF‐1R/Akt/mTOR and ERK1/2 signalling pathways, while PRI inhibited the UM cell viability and attenuated the IGF‐1R downstream signalling activation. This evidence concerns the gene IGF1R and melanoma.