In CRC, KRASG12C/D/V mutations resulted in ROS accumulation, leading to the upregulation of lactate and GM-CSF, thus recruiting macrophages and transforming them into more tumor-supportive tumor-associated macrophages (TAM)-like cells that secreted higher levels of IL-10, CCL17, and TGF-β1 [187]. The gene discussed is TGFB1; the disease is neoplasm.