We recently reported that blocking NK‐1R induces oxidative stress in patients with human myeloid leukemia.[12] However, both HCT116 and SW620 cells treated with SR140333 did not exhibit mitochondrial reactive oxygen species (ROS) or cytosolic ROS accumulation (Appendix A1 and Figure S9, Supporting Information), indicating the cell‐type‐dependent molecular effects of NK‐1R antagonists. The gene discussed is TACR1; the disease is myeloid leukemia.