Problem: Summary of options with respect to TNBC metastasis: Bcl2 activated transcription by estrogen receptor Not applicable to TNBC due to absence of ER. Bcl2 primarily regulates apoptosis, not metastasis directly. Mutation of Ras to RasG12V and MAPK pathway activation Ras mutations and MAPK activation are well-known drivers of proliferation and can promote invasion/metastasis. Common in various cancers but less frequent as a driver mutation specifically in TNBC compared to other breast cancers. GPCR β-arrestin signaling for activation of NF-κB mediated transcription GPCR/β-arrestin pathways activate NF-κB, which strongly promotes inflammation, survival, migration, and metastasis. Emerging evidence implicates this pathway as a key contributor to TNBC metastasis. This pathway also integrates signals that are critical for invasion and metastatic potential. PI3K signaling for the release of second messengers PI3K is central to survival and proliferation, but the phrasing is vague. PI3K pathway is important but less specific to metastasis alone. Current Research Perspective: While Ras/MAPK mutations can promote metastasis, TNBC often exhibits increased GPCR/β-arrestin/NF-κB signaling that more directly drives metastatic behavior. This pathway is considered more specific and directly relevant to TNBC metastasis than the more general Ras mutation option. Final recommendation: GPCR β-arrestin signaling for activation of NF-κB mediated transcription is the best-supported answer. Need Assignment Help?