This aligns with a study showing ABL1/2 drives resistance to BRAF/MEK inhibitors in melanoma[19] and APLP2 decreases HLA class I expression,[20] which is linked to de‐differentiation and resistance to PD‐1 inhibition.[21] Additionally, Figure 3d shows that the expression patterns of these genes in the responding and non‐responding groups are consistent across all cell states, suggesting that these genes are mainly associated with the treatment phenotype rather than cell state. The gene discussed is APLP2; the disease is melanoma.