Using a 5‐aminolevulinic acid (ALA)‐photodynamic therapy model, we have discovered a new effect of nitric oxide (NO)—the ability to accommodate apoptosis. When sensitized by disseminated ALA‐generated protoporphyrin IX, COH‐BR1 tumor cells in glucose‐containing medium died mainly by necrosis with a low level of apoptosis. Introduced before light at a nontoxic concentration, the NO donor SPNO inhibited necrosis, but supported apoptosis such that the latter became predominant in the remaining cell death. Accompanying this was a large increase in caspase‐3/7 activation. SPNO‐supported apoptosis was more pronounced when glucose‐deprived cells were compared with glucose‐replenished, SPNO‐treated counterparts. SPNO plus glucose also suppressed plasma membrane‐damaging lipid peroxidation and loss of cellular ATP under photostress. The NO effect is attributed to membrane protection with maintenance of sufficient glycolytic ATP to sustain apoptosis.