In many cancers, this pathway is overactive due to gain-of-function mutations of phosphatidylinositol-4, 5-bisphosphate 3-kinase, catalytic subunit, alpha (PIK3CA), loss-of-function alterations of the tumor suppressor phosphatase and tensin homolog (PTEN), deregulation of receptor tyrosine kinase signaling, and amplification and mutations of receptor tyrosine kinases [142,143]. Here, NTRK1 is linked to cancer.