Significantly increased expression of PKC-δ and inflammatory mediators with a significant association between the expression of apoptotic regulators cIAP2 and FLIP and pro- and anti-apoptotic markers in BE and EAC tissues suggest that dysregulated programmed cell death, in part, is associated with EAC carcinogenesis and targeting cIAP2 and FLIP seems to be a promising strategy to attenuate the progression of BE and EAC. The gene discussed is PRKCD; the disease is Barrett esophagus.