The other possible mechanism of activity of JNK inhibitors in NB is a disruption in cancer stemness maintained by the STAT3-JNK axis, evidenced by the remarkably lower viability of IMR5, NLF, and SK-N-AS NB cell lines, and the downregulation of the expression of the stem cell marker CXCR4 after treatment with SP600125 or JNK-IN-8 inhibitors [70,71]. The gene discussed is STAT3; the disease is cancer.