In December 2014, the FDA   and the EMA  approved Olaparib as monotherapy, at a recommended dose of 400 mg taken twice per day. The FDA approval is in germline BRCA mutated (gBRCAm) advanced ovarian cancer that has received three or more prior lines of chemotherapy.    The EMA public assessment report, which utilized the same phase II trial data, made reference to both "high grade serous ovarian cancers" and to the use of Olaparib "not later than 8 weeks after a course of platinum -based medicines, when the tumour was diminishing in size or had completely disappeared",  reflecting the phase II trial of Olaparib as maintenance therapy in platinum-sensitive relapsed serous ovarian cancer.   
Defects of the PTEN gene have been cited to be a potential cause of autism spectrum disorders.  When defective, PTEN protein interacts with the protein of a second gene known as Tp53 to dampen energy production in neurons. This severe stress leads to a spike in harmful mitochondrial DNA changes and abnormal levels of energy production in the cerebellum and hippocampus, brain regions critical for social behavior and cognition. When PTEN protein is insufficient, its interaction with p53 triggers deficiencies and defects in other proteins that also have been found in patients with learning disabilities including autism . 
C, EGFR L718Q and L844V Ba/F3 cells retain sensitivity to irreversible quinazoline EGFR inhibitors. Cells were treated with different drugs at the indicated concentrations, and viable cells were measured after 72 hours of treatment and plotted relative to untreated controls. For Western blot analysis, 3T3 cells expressing the respective constructs were treated with different drugs at indicated concentrations for 16 hours. Cell extracts were immunoblotted to detect the indicated proteins. D, EGFR Del 1/L718Q Ba/F3 cells have a growth disadvantage. Equal number of cells was seeded in the presence of or absence of EGF or IL3. Cell number was evaluated in triplicate at the indicated time points.