Altogether these results indicate that the melanoma bias towards MCL1 provides a therapeutic opportunity for combination with multiple ERK1/2 pathway inhibitors, including the clinically approved BRAFV600-mutant selective inhibitor vemurafenib and MEKi such as selumetinib or trametinib, thereby promoting striking tumour cell apoptosis and enhancing tumour growth inhibition in vivo. This evidence concerns the gene MCL1 and neoplasm.