Considering the frequent crosstalk between the PI3K/AKT and RAS/RAF/ERK pathways, and given that Akt/Ras/Raf/MEK/ERK are established therapeutic targets in cancer (44), it is plausible that the coordination between KRAS and TMCC3, potentially through AKT activation, may enhance the RAS/RAF axis of cancer signaling, thereby promoting tumor progression. Here, KRAS is linked to neoplasm.