Interestingly, the changes in STAT3 expression in tumor tissues were identical to those of RNLS, and this consistency from in vitro to in vivo not only reinforces the pathological relevance of the RNLS-STAT3 axis, but also implies that STAT3 may act as an upstream mediator of Ki-67 transcriptional regulation, mediating the pro-carcinogenic effects of RNLS through the activation of proliferation-associated target genes (e. The gene discussed is MKI67; the disease is neoplasm.