We previously reported an extensive biochemical analysis of the impact of UCH-L1 on the mTOR-Akt signaling pathway and found its expression to promote mTORC2 phosphorylation of Akt in three independent myeloma cell lines, in primary B-cells from mice, in HeLa and 293T cells, and in the brain – a mammalian tissue with high levels of endogenous UCH-L1 [21]. This evidence concerns the gene AKT1 and plasma cell myeloma.