Together, our results, at least in cervical cancer cells, establish a concept that in response to growth factors, SHIP2 localizes to the plasma membrane and prevents sustained activation of both PI3K/Akt and MAPK through its lipid phosphatase activity; however, in response to H2O2, it is likely that SHIP2 plays a role as a scaffolding protein to maintain sustained activation of PI3K/Akt and MAPK. The gene discussed is INPPL1; the disease is cervical carcinoma.