BRAF and melanoma: Because a partial reduction in HAT1 protein levels, following the shRNA-mediated HAT1 knockdown in melanoma cells, was unable to cause BRAFi resistance to vemurafenib in a clonogenic long-term survival assay, we generated a complete HAT1 knockout (HAT1-KO) in BRAF-mutant melanoma cells using a clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR associated (Cas)9-based approach29,30.