Other notable genetic alterations include guanine nucleotide-binding protein subunit alpha Q (GNAQ) and guanine nucleotide-binding protein subunit alpha 11 (GNA11) mutations, which are more typical of uveal melanoma rather than cutaneous forms; cyclin dependent kinase inhibitor 2A (CDKN2A) deletions, commonly seen in familial melanoma and some sporadic cases, leading to cell cycle dysregulation; and phosphatase and tensin homolog (PTEN) loss, often coexisting with BRAF mutations, which can contribute to resistance against targeted therapies [82-84]. This evidence concerns the gene PTEN and familial melanoma.