N6-methyl-adenosine (m⁶A) methylation is the most abundant epigenetic modification on mRNA and lncRNA. This modification is regulated by m⁶A writers, readers, and erasers, and its proper regulation is critical for innate and adaptive immunity, especially since m⁶A can play different roles depending on the transcript region, cell type, or specific regulators involved. For example, in the innate immune system, m⁶A can promote the antitumor and antiviral activity of NK cells. It can also activate disease- fighting M1 macrophages, reduce inflammation, and encourage dendritic cell maturation and activity. On the other hand, m⁶A can prevent dendritic cells from cross-presenting tumor antigens to prime T cells, hindering the antitumor response. In the adaptive immune system, m⁶A promotes T cell homeostasis but also suppresses T follicular helper cell development and it can either exacerbate or inhibit HIV-1 infection in CD4⁺ T cells. Furthermore, m⁶A supports B cell development, but it can promote the progression of B-cell lymphoma and it can positively or negatively regulate Kaposi’s sarcoma herpesvirus infection. Given these diverse effects, the exact mechanisms of m⁶A modifications in immunity remain challenging to pinpoint. Nevertheless, with further research, these multifunctional modifications might become valuable therapeutic targets.