Previous reports demonstrate that RBM4 facilitates tumor suppression via not only controlling target pre-mRNA alternative splicing (e.g. Bcl-x and TEAD4) but also through antagonizing oncogenic SRSF1 to inhibit mTOR activation.19,45 Our results reveal that RBM4-S competes with RBM4-FL to elevate SRSF1 protein levels, thus activating mTOR signaling pathway in a dose-dependent manner (Fig. 2m). This evidence concerns the gene TEAD4 and neoplasm.