The ability of Notch signaling to potentiate tumor chemosensitivity by interfering with another cellular metabolic pathway has been reported through in vitro and in vivo studies by Takam Kamga et al. (2018) who showed that Notch4 inhibition increases B-ALL sensitivity to the chemotherapeutic agent ara-C by upregulating the intracellular levels of ROS, which in turn, regulate mTOR, NF-κB, and ERK expression (Takam Kamga et al., 2018). The gene discussed is NOTCH4; the disease is acute lymphoblastic leukemia.