Relevant mechanistic studies have shown that ITPKA promoted cancer cell migration through two different mechanisms: (1) without growth factor stimulation, highly expressed ITPKA binds to F-actin through the N-terminal actin-binding domain (ABD), increasing the polymerization level of cellular F-actin to stabilize microfilaments and subsequently promoting formation of large cellular protrusions [21]. Here, ITPKA is linked to cancer.