Recent studies have explored the underlying mechanisms of adaptive drug resistance in BRAF V600E melanoma.[28] Activation of BRAF downstream pathways (MAPK cascade) or the PI3K‐Akt pathway may occur during BRAF V600E inhibition, leading to cancer refractoriness.[29] These studies shed light on the mechanism underlying BRAF V600E cancer drug resistance, especially in melanoma. This evidence concerns the gene AKT1 and melanoma.