PI3Kα-driven YAP/TAZ activation, possibly through EGF-EGFR-PI3K or FAK–Src–PI3K activation sequences [41,42], is insufficient to promote tumor formation, whereas PI3Kβ-driven YAP/TAZ activation, likely via pertussis toxin-sensitive GPCRs-PI3K activation [43], allows tumor formation [44]. The gene discussed is PIK3CD; the disease is neoplasm.