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Immunoblot analysis has shown that the TMEM106B risk haplotype is associated with increased sarkosyl-insoluble 29 kDa CTF of TMEM106B [83, 164, 165], while decreasing dimeric TMEM106B in the RIPA-soluble fraction [164]

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reported that LKB1 mutation in KRAS mutant lung adenocarcinoma confers a glutamate enriched phenotype in TME, and this feature was associated with CD8 + T cell activation against PD-1, whereas treatment with the glutaminase inhibitor CB-839 inhibited CD8 + T cell expansion and activation