JUN and melanoma: In addition to detecting increased activity of p-ERK1/2T202/Y204 in SHP2-silenced B16F10 tumors compared with controls, the phospho-kinase array showed increased activity of p–c-JunS63 and p–GSK-3bS9,S21/S29, which are mediators of a signaling pathway linking active ERK with increased JNK/c-Jun phosphorylation signaling via stabilization by GSK-3 that is active in progressive melanoma (19).