NF1 and melanoma: The model of class 3 BRAF mutants by Yao et al. [24] postulates that signaling dysregulation by these mutants relies on concomitant mechanisms to support RAS activation: coexisting RAS mutations or NF1 deletions or mutations in melanomas, and RAS activation by aberrant expression or activity of receptor tyrosine kinase in epithelial tumors (lung or CRC).