SP-A is the major surfactant apoprotein exhibiting complex interactions and participation in processes fundamental for pulmonary structure and function with its expression restricted to alveolar epithelial cells type II. Moreover expression of SP-A was also described for a portion of NSCLC facilitating a diagnostic marker for these carcinomas [5, 6] . After characterization of the biochemical properties, a complex chromosomal organization of the genes coding for SP-A has been demonstrated [3] . The locus of the SP-A on the one hand consists of two functionally active genes and a pseudogene [7, 8] . The two active genes SP-A1 and SP-A2 on the other hand display several different alleles and splicing variants, moreover different oligomeric states have been described [3, 9] . During the development of the lung these two genes are regulated differentially, a process triggered by cAMP and glucocorticoids [10] . The SP-A1 and SP-A2 genes display a homology of 94% in their nucleotide sequences and even 96% homology in the amino acid sequences [11] . Fig. 1 , as one example, shows the transcriptional activity of the SP-A1 and SP-A2 genes determined by RT-PCR in homogenates of biopsies from NSCLC and corresponding tumor-free samples. The importance of the differential transcription of SP-A1 and SP-A2 for maintaining pulmonary function has repeatedly been demonstrated [12] . Phylogenetic analyses revealed that an ancestor proto-SP-A gene was diverged into SP-A1 and a second gene which subsequently emerged to SP-A2 and the SP-A pseudogene [3] . The high level of homology between SP-A1 and SP-A2 up to date prevents a differential analysis of the two gene products in situ. The expression of SP-A is also complexly regulated on the transcriptional level. Moreover the protein-turnover and the release of SP-A into the serum represents a further point of regulation [12] . This sophisticated regulation of the genetic activity is recognized as a further hint for the functional importance of SP-A.