For instance, the sequential conversion of PIP3 into PI(3,4)P2 and PI(3)P by Src homology 2-containing inositol 5-phosphatase (SHIP) and INPP4B, respectively, activates SGK3 (Fig. 4b).155–157 PI3K–SGK3 signalling initiated by PI(3)P and INPP4B drives cell proliferation, invasion and tumour growth, demonstrating that phosphoinositides functioning as secondary messengers can dynamically regulate the initiation of different signalling axes, thus providing compensatory pro-tumorigenic effects.155,156. The gene discussed is INPP4B; the disease is neoplasm.