MCL1 and neuroblastoma: Bortezomib-treatment not only caused Mcl1L accumulation, but Mcl1L was also strongly phosphorylated at Ser159 and Thr163 (Fig. 3A), suggesting that the upstream kinase cascades that modulate Mcl1L activity and stability via Ser159/Thr163 phosphorylation are active in these neuroblastoma cells.