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Abstract The (6–4) photolesion is a key photodamage that occurs when two adjacent pyrimidine bases in a DNA strand bond together. To better understand how the absorption of UVB and UVA radiation by the 2‐pyrimidinone moiety in a (6–4) lesion can damage DNA, it is important to study the electronic deactivation mechanism of its 2‐pyrimidinone chromophore. This study employs theoretical (MS‐CASPT2/cc‐pVDZ level) and experimental (steady state and femtosecond broadband spectroscopic) methods to elucidate the photochemical relaxation mechanisms of 2‐(1H)‐pyrimidinone and 1‐methyl‐2‐(1H)‐pyrimidinone in aqueous solution (pH 7.4). In short, excitation at 320 nm leads to the population of the S₁¹(ππ*) state with excess vibrational energy, which relaxes to the S₁¹(ππ*) minimum in one picosecond or less. A trifurcation event in the S₁¹(ππ*) minimum ensued, leading to radiative and nonradiative decay of the population to the ground state or the population of the long‐lived and reactive T₁³(ππ*) state in hundreds of picoseconds. Collectively, the theoretical and experimental results support the idea that in DNA and RNA, the T₁³(ππ*) state of the 2‐pyrimidinone moiety in the (6–4) lesion can further participate in photosensitized chemical reactions increasing DNA and RNA damage.