This project is part of a study aimed at elucidating how Mycobacterium tuberculosis responds to physiologically relevant copper levels during macrophage infection. Here, we conducted a proteomic analysis of macrophages derived from immortalized HoxB8 hematopoietic precursors, in which the Slc31a1 (encoding the Copper transporter 1 or CTR1) or Atp7a (encoding the Copper-transporting ATPase 1) genes were inactivated using CRISPR/Cas9. A luciferase-targeting sgRNA (Luc) served as a control. To validate gene inactivation and evaluate its impact on the macrophage proteome, we systematically compared the proteomic profiles of control (Luc) macrophages with those deficient in CTR1 or ATP7A. Each phenotype was analyzed using four biological replicates, ensuring robust statistical power for downstream analyses.