In a recent attempt to elucidate the role of HIF1α in modulating the fate of T cells, we have demonstrated that the targeted deletion of HIF1α, specifically in T cells, enhances the inflammatory capabilities and memory phenotype of CD8+ T cells. These findings validate that the T cell-specific ablation of HIF1α or pharmacological inhibition of HIF1α reduces the development of B16F10 melanomas, suggesting an improved anti-tumor immune response characterized by improved secretion of effector molecules, such as IFN-γ, granzyme B, and TNFα, in the CD8+ T cells. Thus, it appears that HIF1α might negatively influence specific effector functions of CD8+ T cells, which are crucial for destroying and targeting tumor cells. 

Rickets, a metabolic disease restricted to an age group before epiphyseal growth plate fusion, and is diagnosed by typical skeletal deformities and characteristic radiological features. The commonest etiology of rickets worldwide is nutritional deficiency of vitamin D and/or calcium, followed by primary renal phosphate wasting disorders

Breast Cancer (BCa), a complicated heterogeneous disease, is the most frequent malignancy in females, and it is the leading cancer-related mortality worldwide [1]. Generally, BCa is categorized into three different types based on the presence or absence of molecular biomarkers for (1) estrogen or (2) progesterone receptors and (3) human epidermal growth factor 2 (ERBB2; formerly HER2) [2].