Both PI3K signaling quality (interaction partners, effectors) and quantity (strength, kinetics) differ across contexts, and are under dynamic regulation.
Rather than as a simple ON/OFF cellular switch, the PI3K signaling pathway should be viewed as a highly sensitive dial, whose accurate tuning is a prerequisite for a given cell’s optimal function.
Information transmission within the PI3K signaling pathway is not linear but features complex network properties whose understanding is necessary for successful pharmacological targeting in cancer.
Despite the relatively small number of known (epi)genetic alterations in the PI3K pathway in hematological malignancies, leukemic cells often hijack its functionality for enhanced survival, uncontrolled proliferation and reprogramming of their microenvironment.