Through the interplay of TNF-α and IL-10, Hsp27 is known to haveanti-inflammatory effects.31 Further, while second-generation ASOs havemodifications to allow greater nuclease resistance and increased binding affinitiesthan their predecessors, potential toxicities include hybridisation-dependenttoxicities—due to on- or off-target pharmacology—and hybridisation-independenttoxicities due to nonantisense effects.32 Inhibition of Hsp27 by ASOs, therefore, mayresult in tumour suppression at the expense of increased inflammation. The gene discussed is TNF; the disease is neoplasm.