Consistently, MAPK–ERK activation leads to Cyclin‐B1, c‐myc and Cyclin‐D1 regulation, resulting in increased cell proliferation and accelerated G1 transition, suggesting that the ERK–myc–Cyclin D1 axis can be, at least partly, an oncogenic mechanism by which mortalin contributes to ovarian cancer development and progression. The gene discussed is MYC; the disease is ovarian carcinoma.