Thus, conceivably, the MAPKi act by inhibiting GABP complex transactivation on both TERT mutations, while the non-canonical NF-κB signaling, activated by cytokines and receptors of the tumor necrosis factor receptor (TNFR) superfamily [22], promotes p52/ETS1 binding to the c.-146C > T mutation only, possibly contributing to the worse PFS in these subgroup of MAPKi-treated melanoma patients. The gene discussed is ETS1; the disease is melanoma.