Therefore, it would be tempting to reveal the molecular mechanism by which the PKGI-mediated phosphorylation of IRAG1 inhibits and of IRAG2 activates the intracellular Ca2+ via the IP3R. These mechanisms might also point to new target sites for the development of novel pharmacological modulators of IP3R. Modulators of the IP3R could lead to valuable pharmacological drugs for various diseases, e.g., in the gastrointestinal tract, in the lung, in the heart, in immune cells, or in cancer cells. This evidence concerns the gene IRAG2 and cancer.