The **RAD54L2P1** gene is a pseudogene associated with the RAD54L gene family, which is involved in DNA repair processes. It does not encode a functional protein but may have implications in gene regulation or serve as a source of non-coding RNA.

### 1. Associated Genes
Although RAD54L2P1 is a pseudogene and does not have typical associations as functional genes, it may still be linked to other members of the RAD54 gene family. Notably, **RAD54L** (the functional gene) and other genes involved in DNA repair pathways, such as:
- **BRCA1** (Breast Cancer 1)
- **BRCA2** (Breast Cancer 2)
- **RAD51** (Radiation Sensitive 51)
- **ATM** (Ataxia Telangiectasia Mutated)

### 2. Aging and Age-Related Diseases
As a pseudogene, the direct effects of RAD54L2P1 on aging or age-related diseases are not well-characterized. However, given its association with RAD54L and the broader RAD52 protein family involved in DNA repair, any dysregulation or mutations in these DNA repair systems could theoretically contribute to genomic instability, a hallmark of aging and various age-related diseases, including cancer.

### 3. Drug Interactions
Since RAD54L2P1 is a non-coding pseudogene, there are currently no specific drugs or drug classes directly known to interact with this gene. However, the functioning RAD54L gene could be influenced by treatments that target DNA repair mechanisms, such as:
- **PARP inhibitors** (e.g., Olaparib, Rucaparib), used in certain cancer therapies, particularly involving BRCA mutations.
- **Chemotherapeutics** that induce DNA damage, influencing the activity of DNA repair pathways where RAD54L is functional.

### 4. Pathways and Biological Processes
RAD54L2P1 has a limited role as a pseudogene, but related pathways involving the functional RAD54L include:
- **DNA Repair Mechanisms**, particularly in double-strand break repair.
- **Homologous Recombination** processes, critical for the accurate repair of DNA damage.
- **Cell Cycle Regulation**, wherein proper DNA repair is pivotal to maintaining genomic integrity during cell division.

In summary, while RAD54L2P1 may not actively participate in cellular functions as a pseudogene, its connections to functional DNA repair genes illustrate the complexities of gene families and their potential implications in health and disease. Further research may shed light on indirect influences this pseudogene may have through regulatory mechanisms or interactions with adjacent genes.