Inhibition of ERK1/2 in <i>Smad4<sup>fl/fl</sup></i> ;<i>Kras<sup>G12D</sup></i> mice led to extensive lung SCC formation that resembled the SCC phenotype of <i>Tgfbr2</i>-deficient mice.
The imbalanced expression of MKP-1 and p-ERK(1/2) may play a role in the development of SCC and these two molecules may be new targets for the therapy and prognosis of SCC.