MAPK1 and cervical carcinoma: In this respect, recent data support the hypothesis that toxic substances such as reactive oxygen species may inhibit phosphatases (e.g. protein phosphatase or protein tyrosine phosphatases) and thereby contribute to the activation of ERK (Lee and Esselman, 2002) Another scenario may be that CDDP ligates growth factor receptors, thereby activating the MEK–ERK pathway, as suggested for the cervical carcinoma cell line HeLa (Wang et al, 2000).