Ex vivo and human studies have shown that HCL cells present high levels of MEK and ERK phosphorylation with a reduction in levels induced by inhibitors of BRAF (BRAFi), such as vemurafenib or dabrafenib, suggesting that aberrant signaling through the BRAF–MEK–ERK pathway could be an ideal therapeutic target in HCL [6,7]. The gene discussed is BRAF; the disease is hairy cell leukemia.