The transient effect of Db on p-Erk levels and subsequent increase in p-Akt suggests the ability of 2341 cells to adapt to BRAFV600E inhibition in a manner similar to that seen in melanoma, where mutant BRAF inhibition provides strong selective pressure for upregulation of MAPK and PI3k-Pten-Akt pathways through epigenetic and genetic mechanisms [37]. Here, MAPK1 is linked to melanoma.