CASP9 and coinfection: Notably, this endogenous gcHnf4α-caspase 9 interaction remained consistent across all experimental conditions—unaffected by pathogen type (A. salmonicida or GCRV-II), infection mode (single or co-infection), or pathogenic stimulation itself—indicating a constitutive rather than infection-inducible association that likely functions as a preassembled signaling hub to enable rapid apoptotic activation during microbial challenge.