Table 1.

Table of content.

1. Introduction

2. Non-canonical antagonism by IP4 prevents excessive PI3K signaling in hematopoietic cells

2.1. IP4 limits neutrophil function

2.2. Itpkb limits myelopoiesis from GMP

2.3. Itpkb dampens NK cell function

2.4. Itpkb is required for HSC quiescence and longevity

2.5. Itpkb is required for thymocyte β-selection by dampening Akt/mTORC1 function

3. IP7 may antagonize PI3K in neutrophils

4. IP4 may promote PI3K signaling to enable thymocyte positive selection

5. IP4 dampens store-operated Ca2+ entry (SOCE) in immunocytes to promote survival and prevent inflammatory disease

5.1. Itpkb is required for T cell viability and function

5.2. Itpkc dampens Ca2+ mobilization in immune cells to prevent inflammatory disease

5.3. Itpkb dampens SOCE in B cells

5.4. Itpkb dampens SOCE in neutrophils

6. Does Itpkb inhibition have therapeutic potential in human diseases?

7. Conclusion and Perspectives