Acceleration of cellular aging driven by oxidative stress in COPD lung is characterized by activation of PI3K (phosphoinositide-3-kinase) and mTOR signaling, through oxidation of tyrosine phosphatases such as and SHIP-1 (SH2-containing inositol-59-phosphatase-1) and PTEN (phosphatase tensin homolog) (100). Here, INPP5D is linked to chronic obstructive pulmonary disease.