To accomplish an understanding of how M-CSF-R and AKT activation may contribute to fibrosis, we used a novel transgenic mouse model which expresses a myristoylated and constitutively-active AKT isoform under the control of the M-CSF-R promoter to investigate the connections between cellular CSF1 signaling and the development of pulmonary fibrosis. The gene discussed is CSF1R; the disease is pulmonary fibrosis.