In the case of DUSP5, we previously demonstrated that this phosphatase was a key regulator of nuclear ERK activity and that its deletion accelerated the development of chemically-induced HRASQ61L-driven skin papillomas in mice treated with DMBA/TPA as a result of ERK-dependent up-regulation of SERPINB2 (plasminogen activator inhibitor-2) [14]. The gene discussed is SERPINB2; the disease is skin papilloma.