The functional significance of the non-frameshift substitution (c.700_702CGT) identified in the CtxR 4 cells is unknown; however, in a study focusing on mutations in PIK3R2 and other PI3K pathway-associated genes in endometrial cancer, it was suggested that PIK3R2 mutations may phenocopy loss of the tumor suppressor phosphatase and tensin homolog (PTEN) [49], an alteration that leads to aberrant hyperactivation of PI3K/Akt signaling, which has previously been implicated in cetuximab resistance [3,14,22,26]. This evidence concerns the gene PIK3CA and endometrial cancer.