KRAS-induced autophagic flux supports the survival of tumor cells.70–73 To determine the role of PI4KB in regulating RINCAA and cell proliferation in tumors, we treated two CRC cell lines with different KRAS mutations, such as HCT116 (KRASG13D) and SW620 (KRASG12V), with PIK93 or in combination with the MEK inhibitor trametinib. Here, KRAS is linked to neoplasm.