Our data also suggested that IFN-γ in the responding tumours triggered antiviral and adaptive immune responses through the Jak-STAT signalling pathway (Figure 7) – Among the genes involved in these pathways were CBL, LEPR, SOCS2, SPRY1, and SPRY4, which were downregulated in non-responder melanomas (Table 2) and ultimately contributed to melanoma immune escape. The gene discussed is SOAT1; the disease is neoplasm.