Among RAB GTPases, uncontrolled activation of RAB5 inhibited mTORC1 activity specific to AA stimulation;[21] RAB1 has been identified as a tumorigenic regulator of colorectal cancer and AA promoted RAB1A GTP binding and interaction with mTORC1.[22] In further identification of regulatory network between RAB3B and mTORC1 signaling, we found that RAB3B specifically stimulated the AA‐induced S6 phosphorylation at S235/236. Here, RAB5A is linked to colorectal cancer.