Given the common use of drugs targeting EGFR and other receptor tyrosine kinases (RTKs) operating upstream of PI3K/PTEN in CRC61,62, and the increasing exploration of drugs targeting PI3K and AKT in CRC tumors63–65, a better understanding of PTEN mutational patterns is critical in predicting likely response to these therapeutic agents; the data provided here provide some suggestions into how distinct tumor classes will respond to these agents. The gene discussed is AKT1; the disease is neoplasm.