Twenty-one percent of PIK3CA-mutated cancers also present an FGFR1 amplification.12 These overlapping genetic alterations suggest that combining PI3K or mTOR inhibitors with FGFR TKI to increase cell death may improve the therapeutic activity of these agents.24 This hypothesis is currently being evaluated in a phase-1b clinical trial with the FGFR inhibitor BGJ398 combined with a PI3K inhibitor (BYL719) in FGFR1amp/PIK3CAmut cancers6 (clinicaltrial.gov; NCT01928459). Here, PIK3CA is linked to cancer.