NFKB1 and diabetes mellitus: The p65/50 subunits are the most abundant form of the NF‐κB family, which are inactive and bound to IκB in the cytoplasm of resting cells.42 Once IκB is phosphorylated after diabetic stimuli, the released p65/50 heterodimer then translocates to the nucleus and binds to its target gene promoter.43, 44 Our results showed that kirenol administration efficiently reduced diabetes‐induced phosphorylation of IκBα expression and inhibited the nuclear translocation of the NF‐κB p65 subunit under diabetic stimuli.