Currently, there is mounting evidence from proteomic and transcriptomic studies that the overexpression of Hsp27 is profoundly involved in the gemcitabine resistance to pancreatic cancer whereas, the downregulation of Hsp27, by siRNAs or other molecules that directly inhibit the Hsp27 activity [95], restores the sensitivity to gemcitabine in pancreatic cancer cell lines [96,97,98,99,100,101,102,103,104]. The gene discussed is HSPB1; the disease is pancreatic neoplasm.