Interestingly, we observed that the functional responses to the specific PI3K p110α inhibition were distinct depending on the genetic background for KRAS and PIK3CA. In particular, PIK3CA silencing in CRC cells harboring KRAS/PIK3CA mutations induced apoptosis, as demonstrated by the increased levels of caspase 3/7 activity. The gene discussed is KRAS; the disease is colorectal carcinoma.