These tumours are characterized by a predominant type of T helper cells (Th) with Th1 phenotype (Th1), which potentiate the lytic function of cytotoxic effector T cells present in the tumor microenvironment, activating IFNγ, IL-15 and JAK (Janus kinase)/STAT (signal transducer and activator of transcription) pathways [11, 12]. The gene discussed is IFNG; the disease is neoplasm.