Khanna et al (2011) continued this hypothesis by showing that the MEK1/2 and EGFR inhibitors inhibit CIP2A expression, whereas activation of MEK1/2–ERK signalling pathway stimulates CIP2A expression. They established the ETS1 transcription factor as the mediator of the EGFR–MEK1/2–ERK-induced positive regulation of CIP2A. Our association of CIP2A expression with EGFR protein expression and EGFR gene amplification could provide one putative mechanism for the regulation of CIP2A in human ovarian cancer. This evidence concerns the gene ETS1 and ovarian cancer.