Other mechanisms responsible for HSPs deregulation are: (1) The heat shock factor (HSF) family that ensures prompt transcriptional activation of HSP members under stress and equally precipitous switch-off after recovery [53]; (2) the genetic changes associated with tumor progression, producing over-expressed onco-proteins, mostly mutated and/or conformationally altered proteins, may elicit an HSPs response; (3) the aneuploidy (defined as abnormal chromosome number), and its associated abnormalities [54], such as chromosomal instability (CIN), could impair HSPs expression and function. The gene discussed is PROS1; the disease is cervical squamous intraepithelial neoplasia.