Upregulation of factors such as CSF1 (macrophage colony stimulating factor-1, a cytokine responsible for macrophage production and immunoresponse), CX3CR1 (chemokine signaling), and HLA-DRB (lymphocyte trafficking and T cell receptor signaling), with concurrent modulation of the tumor microenvironment (TME) mediated by increased expression of collagens COL1A1, COL1A2, and COL3A1, may induce an inflammatory niche susceptible to cutting edge therapeutic including immune checkpoint inhibitors. This evidence concerns the gene COL1A1 and neoplasm.