This study investigates the role of dynamic N6-methyladenosine (m6A) mRNA methylation in the translational control of the heat shock response. The research reveals that in response to heat shock stress, m6A is preferentially deposited in the 5' untranslated region (5' UTR) of newly transcribed mRNAs. This dynamic methylation is mediated by the nuclear localization of YTHDF2, a well-characterized m6A "reader" protein. Under heat shock stress, YTHDF2 prevents the m6A "eraser" FTO from demethylating the 5' UTR of stress-induced transcripts, thereby maintaining m6A modification. This increased m6A modification in the 5' UTR promotes cap-independent translation initiation, enabling selective mRNA translation during heat shock stress. The study demonstrates that a single m6A modification in the 5' UTR of Hsp70 mRNA enables translation initiation independent of the 5' end m7G cap. The findings highlight the dynamic nature of 5' UTR methylation and its critical role in cap-independent translation, expanding the physiological roles of m6A and uncovering a novel translational control mechanism in heat shock response. The study also shows that the stress-induced nuclear localization of YTHDF2 is essential for maintaining m6A modification and promoting selective translation. The results suggest that m6A modification acts as a functional cap substitute, enabling cap-independent translation. The study provides insights into the mechanisms underlying the dynamic regulation of m6A modification and its role in stress response.This study investigates the role of dynamic N6-methyladenosine (m6A) mRNA methylation in the translational control of the heat shock response. The research reveals that in response to heat shock stress, m6A is preferentially deposited in the 5' untranslated region (5' UTR) of newly transcribed mRNAs. This dynamic methylation is mediated by the nuclear localization of YTHDF2, a well-characterized m6A "reader" protein. Under heat shock stress, YTHDF2 prevents the m6A "eraser" FTO from demethylating the 5' UTR of stress-induced transcripts, thereby maintaining m6A modification. This increased m6A modification in the 5' UTR promotes cap-independent translation initiation, enabling selective mRNA translation during heat shock stress. The study demonstrates that a single m6A modification in the 5' UTR of Hsp70 mRNA enables translation initiation independent of the 5' end m7G cap. The findings highlight the dynamic nature of 5' UTR methylation and its critical role in cap-independent translation, expanding the physiological roles of m6A and uncovering a novel translational control mechanism in heat shock response. The study also shows that the stress-induced nuclear localization of YTHDF2 is essential for maintaining m6A modification and promoting selective translation. The results suggest that m6A modification acts as a functional cap substitute, enabling cap-independent translation. The study provides insights into the mechanisms underlying the dynamic regulation of m6A modification and its role in stress response.