For example, many blue-pathway tumors (blue nevus/blue melanocytoma and blue nevus-like melanoma) are driven by activating mutations in GNAQ or GNA11 and may acquire additional alterations such as BAP1, SF3B1 or EIF1AX during progression; in this setting, CDKN2A homozygous deletion is not necessarily the dominant event, and p16/MTAP may be less informative. Here, EIF1AX is linked to blue nevus.