PIK3CA and cancer: These mutations address basic cancer cell maintenance requirements: telomere extension by TERT overexpression, cell cycle progression by CDKN2A/B cell cycle-dependent kinase (CDK) 4/6 inhibitors loss and TP53 alterations, the latter being also involved in gatekeeping the DNA-damage response (DDR), and cell survival by inactivation of PTEN, the main inhibitor of the phosphatidyl inositol 3-OH kinase (PI3K) proliferative and anti-apoptotic pathway [3,4].