Through an altered fibrotic phenotype that develops as a result of signaling in the tumor microenvironment, cancer‐associated FBs (CAFs) produce aberrant amounts of HA and collagen I that promote increased TC migration and tumor proliferation.[5] Immunofluorescence analysis of a key marker of CAFs,[27] alpha smooth muscle actin (αSMA), revealed an increasing transformation of FBs into CAFs, especially in the SKBR3, and MDA‐MB‐468 tumoroid microenvironments (Figure 1e). The gene discussed is ACTA1; the disease is cancer.