ITK (IL2-inducible T cell kinase) is a non-receptor tyrosine kinase essential for adaptive immune responses, particularly in T cell development and function. Upon T cell receptor (TCR) activation by antigen-presenting cells, ITK is recruited to the cell membrane and phosphorylated by LCK, leading to its autophosphorylation and full activation. Once activated, ITK phosphorylates downstream effectors including PLCG1, LAT, and LCP2, triggering a signaling cascade that results in calcium mobilization, NFAT nuclear translocation, and ultimately T cell proliferation and differentiation 123. ITK is required for TCR-mediated calcium responses in gamma-delta T cells and regulates both conventional and non-conventional NKT cell development. ITK deficiency has significant clinical relevance. Inherited complete ITK deficiency impairs IFN-γ immunity, causing CD4+ T lymphocytopenia with compensatory expansion of double-negative and gamma-delta T lymphocytes, ultimately underlying severe tuberculosis susceptibility 4. Conversely, ITK deletion in engineered CAR-T cells enhances anti-tumor efficacy by reducing exhaustion signatures, upregulating memory gene expression, and improving cell persistence and tumor control 5. Off-target ITK inhibition occurs with first-generation BTK inhibitors like ibrutinib 67, while second-generation agents show improved selectivity. ITK represents both a critical immune regulator and a promising therapeutic target.