The HATis C646 and anacardic acid, which were toxic in several cell types yet ineffective at repressing LTT expression and MCPyV+ MCC survival, also poorly repressed the p300/CBP-specific H3K27 acetylation in HDFs, indicating that potent inhibition of p300/CBP activity is crucial to targeting MCPyV+ MCC (S2 Fig). This evidence concerns the gene EP300 and Merkel cell skin cancer.