BTZ resistance mechanisms are dependenton tumor-intrinsic and tumor-extrinsic factors.7,38 Forexample, recent studies have elucidated the involvement of mutationsor upregulation of proteasome subunits, particularly β5, inconferring resistance to BTZ,39,40 while other studieshave highlighted the pivotal role of host-mediated pro-tumorigenicresponses.8,9 Specifically, our previous studies haveshown that almost any type of anticancer drug can potentially triggerthe host to upregulate various cytokines and growth factors in theplasma, attracting tumor-supporting cells to the tumor site. Here, CASC3 is linked to neoplasm.