Pyroptosis-related　genes　have　great　potential　for　prognosis,　an　accurate　prognostic　model　based　on　pyroptosis　genes　has　not　been　seen　in　Colorectal　adenocarcinoma　(COAD).　Furthermore,　understanding　the　mechanisms　of　gene　expression　characteristics　and　the　Tumor　Immune　Microenvironment　associated　with　the　prognosis　of　COAD　is　still　largely　unknown.　Constructing　a　prognostic　model　based　on　pyroptosis-related　genes,　and　revealing　prognosis-related　mechanisms　associated　with　the　gene　expression　characteristics　and　tumor　microenvironment.　59　pyroptosis-related　genes　were　collected.　The　gene　expression　data　and　clinical　data　of　COAD　were　downloaded　from　The　Cancer　Genome　Atlas.　External　validation　datasets　were　downloaded　from　the　Gene　Expression　Omnibus　database.　10　characteristic　genes　with　prognostic　values　were　obtained　using　univariate　and　LASSO　Cox.　10-gene　Riskscore　prognostic　model　was　constructed.　Both　gene　set　enrichment　analysis　and　network　propagation　methods　were　used　to　find　pathways　and　key　genes　leading　to　different　prognostic　risks.　The　area　under　the　ROC　curves　were　used　to　evaluate　the　performance　of　the　model　to　distinguish　between　high-risk　and　low-risk　patients,　the　results　were　0.718,　0.672,　and　0.669　for　1-,　3-,　and　5-year　survival　times.　A　nomogram　based　on　Riskscore　and　clinical　characteristics　showed　the　probability　of　survival　at　1,　3,　and　5　years,　and　the　calibration　curves　showed　good　agreement　between　the　predicted　and　actual　observations,　its　C-index　is　0.793.　The　decision　curves　showed　that　the　net　benefit　of　the　nomogram　was　significantly　superior　to　that　of　the　other　single　variables.　Four　key　pathways　leading　to　different　prognostic　risks　were　obtained.　Six　key　genes　with　prognostic　value,　significant　expression　differences　(P　＜　.05)　and　significant　survival　differences　(P　＜　.05)　between　high/low　risk　groups　were　obtained　from　the　gene　set　of　all　4　key　pathways.　This　study　constructed　a　prognostic　model　for　COAD　using　10　pyroptosis-related　genes　with　prognostic　value.　This　study　also　revealed　significant　differences　in　specific　pathways　and　the　tumor　immune　microenvironment　(TME)　between　the　high-risk　group　and　the　low-risk　group,　highlighted　the　roles　of　ALDH5A1　and　Wnt　signaling　in　promoting　COAD　and　the　suppressive　effects　of　the　IL-4/IL-13　pathway　and　RORC　on　COAD.　The　study　will　be　helpful　for　precision　therapy.