Previous studies reported that the PI3K/AKT pathway is activated in about 30% of cervical cancers5,17, and four of six FGFR3-TACC3 fusion-positive cervical cancer samples showed activation of the PI3K–AKT pathway due to copy number amplification or a somatic mutation of at least one gene in the PI3K–AKT pathway (Supplementary Figure 7 and Supplementary Table 5). This evidence concerns the gene AKT1 and cervical carcinoma.