In the second study, three additional BRAFV600E melanoma lines (C32, MM383, and MM386) were profiled by quantitative mass spectrometry following treatment with B18–94, a small-molecule BRN2 inhibitor that disrupts BRN2-DNA binding.63,64 IPA applied to protein-level changes yielded concordantly inverse predictions: among regulators consistently affected across all three lines, MXD1 (a canonical MYC antagonist) was predicted to be inhibited upon BRN2 inhibition, whereas MYC was the top predicted activated regulator, with MYCL and MYCN also activated (Figure 4O). The gene discussed is MYCL; the disease is melanoma.