Similarly to the mechanism described above, the TME is modulated by the interactions between MITF and the c-JUN protein (MITFlow/c-JUNhigh) to produce inflammatory cytokines, inducing melanoma de-differentiation, and subsequently recruiting myeloid immune-suppressive cells into the TME to facilitate tumor progression, resistance to targeted therapies, and metastasis[110,111] [Figure 3]. The gene discussed is MITF; the disease is neoplasm.