FOSL1 and cancer: As recently reviewed [29], in non-transformed cells, FRA-1 is an intrinsically unstable, short-lived protein, while in invasive cancer cells, the increased activity of the RAS/RAF/MEK/ERK pathway induces the phosphorylation of FRA-1 residues S252 and S265, which inhibit the C-terminal (DEST) domain implicated in FRA-1 proteasomal degradation [46].