The same research group more recently validated the hypothesis by demonstrating that in mouse BRAFV600E-driven lung adenocarcinoma, the reduction of intracellular copper content, achieved by CTR1 deletion or by the use of the copper chelator TTM, simultaneously affected autophagic and MAPK signaling, thus leading to the reduction of lung adenocarcinoma growth [114]. This evidence concerns the gene SLC31A1 and lung adenocarcinoma.