And, PHLDA1 augments KRAS pathway activity by stabilizing the RAS–ERK axis: in glioblastoma, PHLDA1 binds to Ras and competitively inhibits Src-mediated Ras phosphorylation, resulting in sustained Ras-GTP levels, increased RAF/MEK/ERK signaling, and elevated downstream MYC transcription; conversely, PHLDA1 knockdown reduces phospho-ERK1/2 levels by approximately 50 % (59). This evidence concerns the gene KRAS and glioblastoma.