These findings conclusively confirm the in silico predictions, highlighting the superior potential of compounds in CRE, particularly C2, in suppressing SRC, STAT3, PIK3CA, MAPK1, EGFR, and JAK1 as proteins involved in the pathways of EGFR tyrosine kinase inhibitors’ resistance in NSCLC. The gene discussed is STAT3; the disease is non-small cell lung carcinoma.