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. This evidence concerns the gene PIK3CD and cancer.