However whilst its growth promoting effects are linked to transactivation of cell cycle target genes such as cyclin D1 [14, 15] and repression of tumour suppressor genes such as BRCA1 [13], its effects in drug treated cells are likely to be driven by activation of the small heat-shock protein, HSP27 [18] which can confer protection against apoptosis and accumulation of DNA damage e.g. caused by reactive oxygen species (ROS) [26, 28]. Here, CCND1 is linked to neoplasm.