PIK3CA and fibrosarcoma: Numerous studies have confirmed that rapidly accelerated fibrosarcoma B-type (BRAF) mutation/fusion, Kirsten rat sarcoma viral oncogene homologue (KRAS) amplification/mutation, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) amplification/mutation, FGFR fusion/amplification, and aberrant alterations in cell-cycle-related genes constitute key acquired resistance mechanisms following osimertinib treatment[39,44] [Figure 2].