CD74 has been reported to play a crucial role in maintaining tumor homeostasis by releasing a signal that inhibits T cell activity, thereby facilitating tumor escape.[34] Additionally, CD44 variants may contribute to the epithelial–mesenchymal transition and adaptive plasticity of cancer cells.[35] We also observed a significant increase in interactions between CD56dim_DNAJB1 and macrophage cells through several ligand-receptor pairs, such as CCL3-CCR1, CCL3L1-CCR1, CCL5-CCR1, IFNG-(IFNGR1+ IFNGR2), IL16-CD4, and TNFSF14-LTBR (Fig. 5F). The gene discussed is IFNG; the disease is neoplasm.