The tumor suppressive function of INPP4B is most likely attributable to the negative regulation of PI3K/AKT signaling, whereas its oncogenic function is still unclear, and promotion of SGK3 signaling, inhibition of phosphatase and tensin homolog (PTEN)- dependent AKT activation, and enhancement of DNA repair mechanisms to confer chemoresistance have been proposed as potential mechanisms [17]. Here, AKT1 is linked to neoplasm.