Kaposi’s sarcoma (KS) is an AIDS-defining cancer and a significant global health challenge caused by Kaposi’s sarcoma-associated herpesvirus (KSHV). NGS-based approaches have profiled KS lesions in a minimal number of studies compared with other neoplastic diseases. Here we present a compiled and harmonized dataset of 131 KS and non-tumor cutaneous samples in the context of their predicted pathway activities, immune infiltrate, KSHV and HIV gene expression profiles, and their associated clinical data representing patient populations from Argentina, United States (USA), and Sub-Saharan Africa cohorts. RNA-seq data from 9 Argentinian KS lesions were generated and integrated with previously published datasets derived from the USA and sub-Saharan African cohorts from Tanzania, Zambia, and Uganda. Unsupervised analysis of 131 KS-related samples allowed us to identify four KS clusters based on their host and KSHV gene expression profiles, immune infiltrate, and the activity of specific signaling pathways. The compiled RNA-seq profile is shared with the research community through the UCSC Xena browser for further visualization, download, and analysis ([https://kaposi.xenahubs.net/](https://kaposi.xenahubs.net/)). These resources will allow biologists without bioinformatics knowledge to explore and correlate the host and viral transcriptome in a curated dataset of different KS RNA-seq-based cohorts, which can lead to novel biological insights and biomarker discovery.

Amyloidosis are a group of diseases in which soluble proteins aggregate and deposit in fibrillar conformation extracellularly in tissues. The effectiveness of therapeutic strategies depends on the specific protein involved, being crucial to accurately determine its nature. Moreover, following the diagnosis, the search for the mutation within relatives allows the clinical advice. Here we report the precise diagnosis and explored the possible reasons of the structural pathogenicity. Whole exome sequencing and GATK calling pipeline were leveraged to characterize the protein variant present in a patient with kidney failure. Bioinformatics strategies were applied to suggest potential explanations of the variants aggregation. Our pipeline allowed the identification of a single point variant of fibrinogen Aα chain, which opened the possibility of curative transplantation. I n silico structural analysis, suggested that the pathogenicity of the variant may be attributed to a heightened susceptibility to yield a peptide prone to deposit as an oligomer with a β-sheet structure. Exploiting the comprehensive coverage of whole genome sequencing we managed to fill a vacant stage in the diagnosis of hereditary amyloidosis and to stimulate the advancement in biomedicine.