It has been hypothesised that BRAF inhibitor induced cutaneous toxicities such as squamous cell carcinoma and keratoacanthoma are caused by keratinocyte proliferation facilitated by the inhibition of wild-type BRAF keratinocytes in the presence of activating RAS mutations, leading to paradoxical activation of MAPK pathway [15–17]. This evidence concerns the gene BRAF and keratoacanthoma.