To further determine the role of ERK1/2 and p38 signaling in controlling the molecular process of SALL1-induced senescence in breast cancer cells, we utilized loss-of-function strategies with specific pharmacological inhibitors and lentivirus-based shRNAs to block ERK1/2 and p38 activities in breast cancer cells, as we previously described [32]. The gene discussed is SALL1; the disease is breast carcinoma.