For this purpose, U2OS cells were transiently transfected with representative disease‐associated MEK1 mutants (F53S, T55P, and Y130C for RASopathies, and K57N and C121S for cancers) and were then treated with etoposide and analyzed for MEK1 cleavage by immunoblotting (Fig. 6A). This evidence concerns the gene MAP2K1 and RASopathy.