However, <47% mucin recovery in ethanol stress-induced models together with effective blocking of H+, K+-ATPase activity in both the models may suggest that, in swim stress, initiation of ulcer pathogenicity may be due to activation of H+, K+-ATPase activity; conversely, in ethanol stress-induced models, it is due to exfoliation and aberrant microcirculation followed by increase in H+, K+-ATPase activity leading to acidity and ulcerations. The gene discussed is MUC5AC; the disease is ulcer disease.