Finally, we highlighted genes (BATF, PRDM1, and TOX) and signalling cascades (JAK-STAT and NF-κB pathways) that extensively engage in multiple branches of T cell anti-tumour responses, outlined preclinical models to validate the efficacy of manipulating resultant genes for augmented cancer immunotherapies, and depicted the prospects of pharmaceutical inhibition and genetic modification to target these genes in the clinic. The gene discussed is SOAT1; the disease is neoplasm.