Immunoblotting of neurofibroma cell lysates after selumetinib treatment showed initial repression of ERK phosphorylation (pERK) and early induction of apoptosis (cleaved Caspase-3, cleaved Caspase-7), followed by recovery of pERK with no change in total protein or mRNA of Ras pathway effectors in cells that persisted despite continued selumetinib treatment (Fig. 2c and Supplementary Fig. 6c). This evidence concerns the gene CASP3 and plexiform neurofibroma.