Figure illustrates our results from the co-occurrence analysis of emerging concepts in immunooncology focused on various types of therapeutic targets and cancer types. Highlighted below are a few interesting co-occurring pairs many of which involve N6-methyladenosine (m 6 A). We have chosen candidates from both ends of the spectrum: those with high average fold increase but relatively low number of publications (m A | lung cancer, m A | liver cancer, TAMs | ovarian cancer, CD8 | colon cancer, PD-1 | colorectal cancer and HER2 | NSCLC) indicative of recent growing interest (and hence emergence), as well as concept pairs with relatively lower average fold increase but with a large number of publications (PD-1 | liver cancer, PD-L1 | gastric cancer) N6-Methyladenosine (m 6 A) is a type of reversible RNA modification that is achieved using combination of "writers", "readers" and "erasers". The dysregulation of m6A may lead to tumorigenesis and progression, making m6A regulators potential clinical therapeutic targets for cancers. • m 6 A | Lung cancer A prevalent and dynamic RNA modification, N6-methyladenosine (m 6 A), plays a crucial role in various biological processes, including mRNA stability, splicing, translation, and degradation. Recent research has highlighted the significance of m 6 A modification in cancer biology, including lung cancer, where it influences tumor development, progression, and response to therapy. Emerging studies have demonstrated that dysregulation of m 6 A is involved in many diseases, especially pulmonary tumorigenesis and progression. m 6 A modifications can contribute to drug resistance in lung cancer. For example, alterations in m A levels can affect the sensitivity of lung cancer cells to chemotherapeutic agents or targeted therapies such as epidermal growth factor receptor (EGFR) inhibitors. Understanding these mechanisms may help in developing strategies to overcome resistance. m 6 A modifications can influence the tumor immune microenvironment by regulating the expression of immune checkpoint molecules and cytokines. This can impact the efficacy of immunotherapies, such as PD-1/PD-L1 inhibitors, in lung cancer treatment. m A regulators and modified mRNAs can serve as potential biomarkers for lung cancer diagnosis, prognosis, and treatment response. For instance, high levels of METTL3 expression have been associated with poor prognosis in lung cancer patients. The m 6 A | lung cancer concept pair co-occurrence exhibits the highest average fold increase in publications (nearly 4.5-fold) of all therapeutic target and cancer type concept pairs (Figure ) which spotlights it as a truly emerging topic in immuno-oncology. Of note, the pair shows a marked increase in publications after 2019, growing by 8-fold over a two-year period (Supporting Information S1). m A methylation is also critical in the context of liver cancer, particularly HCC, the most common type of liver cancer, influencing tumor biology and the immune response. Key m 6 A regulators, including methyltransferases (writers such as METTL3 and METTL14), demethylases (erasers such as FTO and ALKBH5), and m 6 A-binding proteins (readers such as YTHDF1-3), play critical roles in HCC cell proliferation and survival. For instance, METTL3mediated m A modification has been shown to enhance the stability of mRNAs that promote HCC progression. m 6 A modifications can regulate the Epithelial-Mesenchymal Transition (EMT) process, which is essential for cancer metastasis. Changes in m A levels can influence the expression of EMTrelated genes, thereby affecting the invasive and metastatic potential of HCC cells. m 6 A modifications play a role in maintaining the stemness 39 of cancer stem cells, which are implicated in HCC initiation and recurrence. For example, METTL3 can enhance the expression of stemness-related genes, contributing to the self-renewal capacity of CSCs. m 6 A modifications can influence the immune microenvironment of HCC by regulating the expression of immune-related genes and cytokines. This can impact the response to immunotherapies, such as checkpoint inhibitors, in HCC treatment. While the m 6 A | liver cancer concept pair exhibits a lower average growth rate (around 3-fold) as compared to the m 6 A | lung cancer concept pair, the growth in publications shows a decidedly upward trend increasing by 11-fold over 2020-2022 (Supporting Information S2).