[11] In addition, Su et al. confirmed that mutations in RAS, particularly HRAS, are frequent in keratoacanthomas and squamous cell carcinomas in patients treated with Vemurafenib. [20] They have elegantly demonstrated that activated RAS will result in a paradoxical activation of MAPK signaling accelerating tumor growth in BRAF wild type lesions. This suggests that RAS activation is the key event for the progression of keratoacanthomas and squamous cell carcinomas. Homodimer and heterodimer formation involving all members of the BRAF family seems to be involved. [21]–[23]. This evidence concerns the gene HRAS and neoplasm.