According to Lian et al., HNRNPC facilitated the expression of TFAP2A and subsequently the transcription of DDR1 by recognizing the m6A modification of TFAP2A mRNA mediated by VIRMA—these mainly through potentiating the TFAP2A/DDR1 axis and promoting collagen fiber alignment, thus decreasing the infiltration of antitumor immune cells and fostering immune evasion in BC [110]. The gene discussed is TFAP2A; the disease is breast cancer.