PIK3CB and neoplasm: Considering that PI3K signaling pathways always show particularly high activity in cancers and that PI3K subunits are frequently mutated or truncated, which may be, at least in part, a reason for the enhanced functions of the PI3K pathways during the course of tumor metagenesis and deterioration [51–54], and as Western blot analysis results showed this truncation in the KB-C2 cells but not the parental KB-3-1 cells, it is possible to design more specific knockouts based on the sequence of mutated PI3K subunits in cancer cells without interfering with the PI3K genes in normal tissues.