To that end, since the original discovery of KRAS mutations in human lung cancer cells (Capon et al., 1983), it has emerged that ~75% of LUADs display mutational activation of key components of receptor tyrosine kinase (RTK) signaling that, in turn, promote activation of RAS and its key downstream effectors: the RAF→MEK→ERK→MAP kinase (MAPK) and the PI3’-lipid pathways (Cancer Genome Atlas Research Network, 2014; Heist and Engelman, 2012). The gene discussed is PI3; the disease is lung carcinoma.