Ifng, encoding Interferon gamma, is a key cytokine in the immune system. It plays a crucial role in enhancing immune function, such as promoting the activation of immune cells. It is involved in multiple pathways, including those related to immune responses against pathogens and in cancer immunology. Its dysregulation is associated with various diseases, highlighting its biological importance. Genetic models, like gene knockout (KO) or conditional knockout (CKO) mouse models, can be valuable for studying Ifng's functions [2-10].

In autism spectrum disorder (ASD) children, there is a significant up-regulation of Ifng compared to controls, indicating a disruption in the IFNG/IFNG-AS1 regulatory network which may contribute to ASD's chronic inflammatory aspect [1]. In colon adenocarcinoma (COAD), Ifng is significantly correlated with tumor immunotherapy biomarkers, and high Ifng expression is related to longer disease-free survival. Also, autophagy and Ifng are negatively related to cisplatin chemosensitivity [2]. Regarding tuberculosis, Ifng gene polymorphisms show associations with the disease in the Tibetan population, with certain alleles acting as protective or risk factors [3,4]. In atopic dermatitis, high and low Ifng-expressing subgroups have distinct features, corresponding to intrinsic and extrinsic AD classifications [5]. Cholesterol can promote Ifng mRNA expression in CD4+ effector/memory cells via SGK1 activation [6].

In summary, Ifng is essential for immune function and is implicated in multiple disease conditions including ASD, COAD, tuberculosis, and atopic dermatitis. Model-based research, such as through KO/CKO mouse models, can further reveal its functions in these diseases, providing insights into disease mechanisms and potential therapeutic targets.