Focusing on the loss-of-function mutations (Fig. 5B), a loss of cJUN, Sp1, and Ets-1 function, which are key to TNF-α production in the model, promoted residency of LCs irrespective of the genetic background of the melanomas, while loss of signaling via the TNF receptor enhanced residency only in MITFhigh backgrounds. The gene discussed is JUN; the disease is melanoma.