This microenvironment poses a series of metabolic hurdles for T cells: (i) hypoxia in poorly vascularized tumor areas can affect T cell functions also through HIF1α induction; (ii) lactate released by both tumor and stromal cells, and the consequent extracellular acidity, can profoundly suppress the effector functions of T cells and compromise anti-tumor immunity; and (iii) the capture of nutrients (glucose, amino acids, and fatty acids) by tumor and stromal cells generates a status of metabolic restriction that ultimately leads to T cell starvation (107). Here, HIF1A is linked to neoplasm.