IL-1 production by melanoma cells can suppress FRC contractility through JAK1/STAT3 pathway inhibition, with the consequent relaxation of the 3D FRC network, better-enabling melanoma cells to invade this niche.85 Transcriptional analyses of FRCs in TDLNs have provided evidence of microenvironmental reprogramming, including the expansion and structural reorganization of stromal compartments and the suppression of CCL21 and IL-7 production by FRCs, enabling greater tumor cell immune evasion and impaired immune cell homing.86 This evidence concerns the gene IL1B and melanoma.